DOCSLIB.ORG

Endotoxins in Swine – Effects and Strategies for Control

Total Page：16

File Type：pdf, Size：1020Kb

Download full-text PDF Read full-text
Endotoxins in Swine – Effects and Strategies for Control Endotoxins in swine – effects and strategies for control by Josep Garcia-Sirera, Special extremely sensitive to detergents, antibiotics Nutrients Inc, 2766 Douglas Road, and bile salts. So it seems that this region is Cocunut Grove, Florida 33133, USA. essential for the maintenance of outer mem - brane functions as a biological barrier. ndotoxins are structural components Mutations altering the lipid A component of bacteria. They are part of the outer are mostly not viable, suggesting that it is Emembrane of Gram negative bacteria, important for the maintenance of outer which are released mainly when bacteria are membrane integrity as a whole. lysed, due to the use of antibiotics or because of the body’s defence mechanism. Together with phospholipids and mem - Lipid A and virulence brane bound proteins they are constituents of the outer cell membrane. The typical The physiological activities of LPS are medi - Fig. 2. Schematic view of the cellular structure of an endotoxin consists of a ated mainly by the lipid A component of endotoxin (LPS) signal transduction lypopolysaccharide (LPS). These LPS define LPS. Lipid A is a powerful biological pathway. LPS binding protein (LBP) many of the properties of host-parasite response modifier that can stimulate the mammalian immune system. During infec - solved in the plasma ligates at LPS (1). interactions. This complex binds to the cell surface tious disease caused by Gram negative bac - LPS consists of three structural elements. receptor CD14 (2). Aggregation of teria, endotoxins released from, or part of, One is a hydrophobic component, called LBP/LPS/CD14 complex with the protein multiplying cells have similar effects on ani - lipid A, which serves to anchor the molecule MD2 and the transmembrane toll like mals and significantly contribute to the into the membrane. The second is a core receptor (TLR) 4 (3) induces the signal symptoms and pathology of the disease oligosaccharide. The third component is a transduction cascade in the cell (4, 5). hydrophilic O-polysaccharide projecting into encountered. Finally, transcription factor NF κB is acti - the extracellular space. More than 150 dif - Since lipid A is embedded in the outer vated (6) and starts translation of sev - ferent variants of the third component are membrane of bacterial cells, it probably only eral genes to proteins, for example known. The O-polysaccharide portion exerts its toxic effects when the bacteria are pro-inflammatory mediators like IL-1 β seems to be relevant to host-parasite inter - lysed as a result of autolysis and the mem - (7,8). actions because its disappearance results in brane attack complex (MAC), ingestion and loss of virulence. killing by phagocytes, or killing with certain The loss of the proximal part of the core types of antibiotics. tein, MD2, which associates with toll-like oligosaccharide induces bacteria to become The injection of living or killed Gram nega - receptor-4 (TLR4). tive cells or purified LPS into experimental This triggers the signaling cascade for Fig. 1. Lypopolysaccharide structure. animals causes a wide spectrum of non-spe - macrophage/endothelial cells to secrete cific pathophysiological reactions, such as pro-inflammatory cytokines and nitric oxide fever, changes in white blood cell counts, that lead to the characteristic ‘endotoxic disseminated intravascular coagulation, shock’. hypotension, shock and death. Injection of CD14 and TLR4 are present on several fairly small doses of endotoxin results in cells of the immunological system, including death in most mammals. macrophages and dendritic cells. The sequence of events follows a regular In monocytes and macrophages, three pattern: types of events are triggered during their G Latent period. interaction with LPS: G Physiological distress (diarrhoea, prostra - G Production of cytokines, including IL-1, tion, shock). IL-6, IL-8, tumour necrosis factor (TNF) and G Death. platelet activating factor. These, in turn, How soon death occurs varies on the stimulate production of prostaglandins and dose of the endotoxin, route of administra - leukotrienes. These are powerful mediators tion, and species of animal. Animals vary in of inflammation and septic shock that their susceptibility to endotoxin and the accompanies endotoxin toxaemia. LPS acti - mechanism is complex. vates macrophages to enhanced phagocyto - In humans, LPS binds to a lipid binding pro - sis and cytotoxicity. Macrophages are tein (LBP) in the serum which transfers it to stimulated to produce and release lysosomal CD14 on the cell membrane, which in turn enzymes, IL-1 (‘endogenous pyrogen’), and transfers it to another non-anchored pro - Continued on page 14 International Pig Topics — Volume 25 Number 3 13 Continued from page 13 Treatment Final ADG Feed CI tumour necrosis factor (TNFalpha), as well weight (g) (g) intake (g/d) as other cytokines and mediators. Activation of the complement cascade. G Control 749.68±14.16 a 33.61±0.66 a 44.96±0.88 a 1.388±0.010 b C3a and C5a cause histamine release (lead - b b ab a ing to vasodilation) and affect neutrophil LPS 684.63±16.81 30.51±0.79 42.58±0.97 1.396±0.018 chemotaxis and accumulation. The result is YCL 744.40±19.12 a 33.35±0.91 a 44.28±1.04 a 1.328±0.012 b inflammation. LPS + YCL 692.93±8.25 b 30.91±0.38 b 41.56±0.58 b 1.344±0.014 b G Activation of the coagulation cascade. Initial activation of Hageman factor (blood- Means in the same column with a different letter are statistically different (P<0.05) clotting Factor XII) can activate several Table 1. Effect of inclusion of yeast cell wall in the diet on production parameters humoral systems resulting in: (1-21 days) of broilers inoculated with LPS of E. coli (Badia R. et al). – coagulation: a blood clotting cascade that leads to coagulation, thrombosis, acute dis - – activation of the complement alternative – kinin activation releases bradykinins and seminated intravascular coagulation, which pathway (which leads to inflammation). other vasoactive peptides which causes depletes platelets and various clotting fac - – plasmin activation which leads to fibrinoly - hypotension. tors resulting in internal bleeding. sis and haemorrhaging. The net effect is to induce inflammation, intravascular coagulation, haemorrhage and shock. LPS also acts as a B cell mitogen, stimulating the polyclonal differentiation and multiplication of B-cells and the secretion of immunoglobulins, especially IgG and IgM. Control of endotoxins In general, strategies to control endotoxin contamination in animals include all of those aimed at the reduction of bacterial contami - nation. These strategies include, but are not limited to, biosecurity, use of prebiotics, probiotics and improved nutrient digestibil - ity. Other strategies such as vaccination and use of toxin binders specifically target endo - toxin contamination. G Vaccination. As explained before, the lipid A portion is responsible for endotoxin toxicity. Also it is the more consistent por - tion of LPS structure. Currently, immunisa - tion against lipid A is being developed, but the high cost makes it a non-viable option for livestock production. Another option considered in vaccination is to immunise against LBP, in an attempt to reduce the formation of LBS-LBP complex that initiates the cascade of events leading to pathogenesis. This option is also expensive and currently only to be considered for human use. G Immunity modulators. Use of immune modulators to compensate the effects of endotoxins have been tested in animal pro - duction. In broilers, inoculation with LPS induces an activation of the immune system. Some studies show that broilers inocu - lated with LPS decrease productivity. This reduction is related to the action of inter - leukins produced during the acute inflamma - tory phase. On the other hand, some studies show the immune-modulating action of B-glucans present in yeast cell wall. Table 1 shows the results of using yeast cell wall (YCL) in diet of broilers inoculated with LPS. YCL was capable of counteracting the effect of LPS in conversion index (CI). Further tests would be needed to study the possibility of using immune modulators against endotoxins. A more practical approach to reduce absorption of endotoxins from the gastroin - testinal tract of livestock is the use of toxin 14 International Pig Topics — Volume 25 Number 3 binders. Toxin binders are widely used to against endotoxins in swine. Fig. 3 shows the control other toxins such mycotoxins. 35 Control AZ 0.05% AZ 0.10% results of using a commercially available The binder and the mycotoxin form a toxin binder to reduce free endotoxin con - complex that is too large to be absorbed 30 centration in endotoxin producing bacterial into the blood system. The complex is then cell culture. eliminated in the faeces. 25 The product was capable of binding endo - Most mycotoxin binders are hydrophilic toxins at two different inclusion rates. This 20 molecules (bentonites, aluminosilicates) effi - binding capacity was confirmed in an in vivo cient at capturing polar molecules such as test. 15 aflatoxin. The capacity of these traditional Table 2 shows free endotoxin concentra - mycotoxin binders to capture more 10 tion in blood of sows before and after feed - lipophilic-like molecules such zearalanenone ing them the commercial toxin binder or DON is questionable. There are also 5 This preliminary data suggest that the toxin organic mycotoxin binders (MOS based) binder is capable of binding endotoxin and that claim to be able to adsorb a wider 0 the gastrointestinal tract, and thus prevent - range of mycotoxins. Farm 1 Farm 2 ing endotoxins from being absorbed. Further studies are currently underway to Fig. 3. Endotoxin concentration in bac - further test this product. Table 2. Endotoxin concentration in terial cell culture of sow faeces (1-2pp) blood of sows before and after (three after in vitro supplementation of differ - weeks) addition (1kg/MT of feed) of ent MycoAD AZ concentrations (Univ- Summary MycoAD AZ (Biocheck, Leipzig, ersity of Leipzig).
Load more

Recommended publications
  • Pathological and Therapeutic Approach to Endotoxin-Secreting Bacteria Involved in Periodontal Disease
    toxins Review Pathological and Therapeutic Approach to Endotoxin-Secreting Bacteria Involved in Periodontal Disease Rosalia Marcano 1, M. Ángeles Rojo 2 , Damián Cordoba-Diaz 3 and Manuel Garrosa 1,* 1 Department of Cell Biology, Histology and Pharmacology, Faculty of Medicine and INCYL, University of Valladolid, 47005 Valladolid, Spain; [email protected] 2 Area of Experimental Sciences, Miguel de Cervantes European University, 47012 Valladolid, Spain; [email protected] 3 Area of Pharmaceutics and Food Technology, Faculty of Pharmacy, and IUFI, Complutense University of Madrid, 28040 Madrid, Spain; [email protected] * Correspondence: [email protected] Abstract: It is widely recognized that periodontal disease is an inflammatory entity of infectious origin, in which the immune activation of the host leads to the destruction of the supporting tissues of the tooth. Periodontal pathogenic bacteria like Porphyromonas gingivalis, that belongs to the complex net of oral microflora, exhibits a toxicogenic potential by releasing endotoxins, which are the lipopolysaccharide component (LPS) available in the outer cell wall of Gram-negative bacteria. Endotoxins are released into the tissues causing damage after the cell is lysed. There are three well-defined regions in the LPS: one of them, the lipid A, has a lipidic nature, and the other two, the Core and the O-antigen, have a glycosidic nature, all of them with independent and synergistic functions. Lipid A is the “bioactive center” of LPS, responsible for its toxicity, and shows great variability along bacteria. In general, endotoxins have specific receptors at the cells, causing a wide immunoinflammatory response by inducing the release of pro-inflammatory cytokines and the production of matrix metalloproteinases.
    [Show full text]
  • Instability of Toxin a Subunit of AB5 Toxins in the Bacterial Periplasm Caused by Deficiency of Their Cognate B Subunits
    Biochimica et Biophysica Acta 1808 (2011) 2359–2365 Contents lists available at ScienceDirect Biochimica et Biophysica Acta journal homepage: www.elsevier.com/locate/bbamem Instability of toxin A subunit of AB5 toxins in the bacterial periplasm caused by deficiency of their cognate B subunits Sang-Hyun Kim a, Su Hyang Ryu a, Sang-Ho Lee a, Yong-Hoon Lee a, Sang-Rae Lee a, Jae-Won Huh a, Sun-Uk Kim a, Ekyune Kim d, Sunghyun Kim b, Sangyong Jon b, Russell E. Bishop c,⁎, Kyu-Tae Chang a,⁎⁎ a The National Primate Research Center, Korea Research Institute of Bioscience and Biotechnology (KRIBB), Ochang, Cheongwon, Chungbuk 363–883, Republic of Korea b School of Life Science, Gwangju Institute of Science and Technology (GIST), 1 Oryong-dong, Gwangju 500–712, Republic of Korea c Department of Biochemistry and Biomedical Sciences, McMaster University, Hamilton, Ontario, Canada L8N 3Z5 d College of Pharmacy, Catholic University of Daegu, Hayang-eup, Gyeongsan, Gyeongbuk 712-702, Republic of Korea article info abstract Article history: Shiga toxin (STx) belongs to the AB5 toxin family and is transiently localized in the periplasm before secretion Received 26 April 2011 into the extracellular milieu. While producing outer membrane vesicles (OMVs) containing only A subunit of Received in revised form 3 June 2011 the toxin (STxA), we created specific STx1B- and STx2B-deficient mutants of E. coli O157:H7. Surprisingly, Accepted 23 June 2011 STxA subunit was absent in the OMVs and periplasm of the STxB-deficient mutants. In parallel, the A subunit Available online 5 July 2011 of heat-labile toxin (LT) of enterotoxigenic E.
    [Show full text]
  • Mycotoxin Analysis in Infant Formula Using Captiva EMR-Lipid
    Application Note Food Testing & Agriculture Mycotoxin Analysis in Infant Formula Using Captiva EMR—Lipid Cleanup and LC/MS/MS Author Abstract Derick Lucas Agilent Technologies, Inc. Several countries regulate the levels of mycotoxins in foods. However, the complexity of certain foodstuffs in terms of protein and lipid content can prove challenging in the accurate quantitation of low-level mycotoxins in these matrices. This Application Note describes the determination of 13 multiclass mycotoxins in solid and liquid infant formulations using a Quick Easy Cheap Effective Rugged Safe (QuEChERS) workflow followed by Agilent Captiva EMR—Lipid cartridge cleanup. Due to the high selectivity of the Captiva EMR—Lipid sorbent, excellent recoveries (70.4 to 106.8 %) and precision (<18 %) were achieved for all mycotoxins. This simple and robust methodology requires minimal equipment and expertise, which promotes easy implementation in food laboratories. Introduction Experimental Mycotoxins are produced as secondary metabolites by fungal Sample preparation species that grow on various crops such as grain, corn, and • Captiva EMR—Lipid 3-mL tubes (p/n 5190-1003) nuts. When cows ingest contaminated feed, mycotoxins and their metabolites can be excreted into the animal’s milk1. • Captiva EMR—Lipid 6-mL tubes (p/n 5190-1004) Aflatoxin M1 is the most commonly found mycotoxin in milk, • QuEChERS original extraction salts (p/n 5982-5550) and is monitored and regulated in many countries, including • VacElut SPS 24 vacuum manifold (p/n 12234022) the United States and European countries2,3. Despite a lack of regulations for other mycotoxins in milk, there is a growing LC configuration and parameters interest to monitor additional mycotoxins such as fumonisins and ochratoxins.
    [Show full text]
  • Impact of Bacterial Toxins in the Lungs
    toxins Review Impact of Bacterial Toxins in the Lungs 1,2,3, , 4,5, 3 2 Rudolf Lucas * y, Yalda Hadizamani y, Joyce Gonzales , Boris Gorshkov , Thomas Bodmer 6, Yves Berthiaume 7, Ueli Moehrlen 8, Hartmut Lode 9, Hanno Huwer 10, Martina Hudel 11, Mobarak Abu Mraheil 11, Haroldo Alfredo Flores Toque 1,2, 11 4,5,12,13, , Trinad Chakraborty and Jürg Hamacher * y 1 Pharmacology and Toxicology, Medical College of Georgia at Augusta University, Augusta, GA 30912, USA; hfl[email protected] 2 Vascular Biology Center, Medical College of Georgia at Augusta University, Augusta, GA 30912, USA; [email protected] 3 Department of Medicine and Division of Pulmonary Critical Care Medicine, Medical College of Georgia at Augusta University, Augusta, GA 30912, USA; [email protected] 4 Lungen-und Atmungsstiftung, Bern, 3012 Bern, Switzerland; [email protected] 5 Pneumology, Clinic for General Internal Medicine, Lindenhofspital Bern, 3012 Bern, Switzerland 6 Labormedizinisches Zentrum Dr. Risch, Waldeggstr. 37 CH-3097 Liebefeld, Switzerland; [email protected] 7 Department of Medicine, Faculty of Medicine, Université de Montréal, Montréal, QC H3T 1J4, Canada; [email protected] 8 Pediatric Surgery, University Children’s Hospital, Zürich, Steinwiesstrasse 75, CH-8032 Zürch, Switzerland; [email protected] 9 Insitut für klinische Pharmakologie, Charité, Universitätsklinikum Berlin, Reichsstrasse 2, D-14052 Berlin, Germany; [email protected] 10 Department of Cardiothoracic Surgery, Voelklingen Heart Center, 66333
    [Show full text]
  • Host-Based Lipid Inflammation Drives Pathogenesis in Francisella Infection
    Host-based lipid inflammation drives pathogenesis in Francisella infection Alison J. Scotta, Julia Maria Postb, Raissa Lernerb, Shane R. Ellisc, Joshua Liebermand, Kari Ann Shireye, Ron M. A. Heerenc, Laura Bindilab, and Robert K. Ernsta,1 aDepartment of Microbial Pathogenesis, School of Dentistry, University of Maryland, Baltimore, MD 21201; bLaboratory for Eicosanoids and Endocannabinoids, Johannes Gutenberg University Mainz, 55099 Mainz, Germany; cMaastricht MultiModal Molecular Imaging Institute, Maastricht University, 6229 ER Maastricht, The Netherlands; dDepartment of Pathology, University of Washington Medical Center, Seattle, WA 98118; and eDepartment of Microbiology and Immunology, School of Medicine, University of Maryland, Baltimore, MD 21201 Edited by Roy Curtiss III, University of Florida, Gainesville, FL, and approved October 16, 2017 (received for review July 19, 2017) Mass spectrometry imaging (MSI) was used to elucidate host lipids MSI (18), although other ionization methods [such as desorption involved in the inflammatory signaling pathway generated at the electrospray ionization (DESI) and liquid extraction surface host–pathogen interface during a septic bacterial infection. Using analysis (LESA), and others] are also employed. MSI has been Francisella novicida as a model organism, a bacterial lipid virulence used in a wide array of applications ranging from fingerprint factor (endotoxin) was imaged and identified along with host phos- analysis to mapping drug distribution in tissue. MSI studies of pholipids involved in the splenic response in murine tissues. Here, cancer biology for biomarker discovery, therapeutic target iden- we demonstrate detection and distribution of endotoxin in a lethal tification, and fundamental pathology hold particular promise. In murine F. novicida infection model, in addition to determining the contrast, comparatively few systematic studies have leveraged MSI – temporally and spatially resolved innate lipid inflammatory response to describe the host microbe relationship (19, 20).
    [Show full text]
  • Determination of Lipid a and Endotoxin in Serum by Mass Spectroscopy (Ft-Hydroxymyristic Acid/Gas Chromatography-Mass Spectrometry/Gram-Negative Sepsis) SHYAMAL K
    Proc. Nati. Acad. Sci. USA Vol. 75, No. 8, pp. 3993-3997, August 1978 Medical Sciences Determination of lipid A and endotoxin in serum by mass spectroscopy (ft-hydroxymyristic acid/gas chromatography-mass spectrometry/Gram-negative sepsis) SHYAMAL K. MAITRA*t, MICHAEL C. SCHOTZtf, THOMAS T. YOSHIKAWA*t, AND LUCIEN B. GUZE*tl * Research Service, Veterans Administration, Wadsworth Hospital Center, Los Angeles, California 90073; * Departments of Medicine, Harbor General Hospital, Torrance, California 90509; and t UCLA School of Medicine, Los Angeles, California 90024 Communicated by William N. Valentine, June 1, 1978 ABSTRACr A quantitative technique for determining lipid tography-mass spectrometry. Mass spectrometry has been used A content of endotoxin added to serum by combined gas chro- successfully in the past to detect various biological compounds matography-mass spectrometry is described. This technique uses (26). This procedure is highly specific and very sensitive. detection of the -hydroxymyristic acid content of Salmonella The minnesota R595 lipopolysaccharide by selected ion monitoring method described in this communication quantitates nanogram at atomic mass unit of 315.4 The fatty acids produced on hy- quantities of lipid A and endotoxin in serum. drolysis of serum containing lipopolysaccharide were extracted and the methyl esters were made. Silica gel chromatography was MATERIALS AND METHODS used to separate methyl esters of hydroxy fatty acids from other Serum Samples. New Zealand white rabbits weighing ap- fatty acid methyl esters. Trimethylsilyl ether derivatives of the proximately 2 kg, and not fed overnight, were used. Blood was hydroxy fatty acid methyl ester fraction were quantitated by this technique. As little as 200 fmol of fi-hydroxymyristic acid obtained by heart puncture under sterile conditions.
    [Show full text]
  • LIPID MEDIATORS in HEALTH and DISEASE II: from the Cutting Edge–A Tribute to Edward Dennis and 7TH INTERNATIONAL CONFERENCE on PHOSPHOLIPASE A2 and LIPID MEDIATORS
    LIPID MEDIATORS IN HEALTH AND DISEASE II: From The Cutting Edge–A Tribute to Edward Dennis And 7TH INTERNATIONAL CONFERENCE ON PHOSPHOLIPASE A2 and LIPID MEDIATORS: From Bench To Translational Medicine Honorary Chair: Nobel Laureate Bengt Samuelsson La Jolla, California May 19-20, 2016 http://www.medschool.lsuhsc.edu/neuroscience/LipidMediatorsPLA2-2016/ Lipid Mediators in Health and Disease II: From The Cutting Edge • A Tribute to Edward Dennis 2+ Steered molecular dynamics simulation of Group VIA Ca - independent phospholipase A2 (PLA2) embedded in a bilayer membrane composed mainly of 1-palmitoyl, 2-oleoyl phosphatidycholine (POPC) extracting and pulling a 1-palmitoyl, 2-archidonyl phosphatidylcholine (PAPC) into its binding pocket in the active site. [For movies of this simulation, see Mouchlis VD, Bucher, D, McCammon, JA, Dennia EA (2015) Membranes serve as allosteric activators of phospholipase A2 enabling it to extract, bind, and hydrolyze phospholipid substrates, Proc Natl Acad Sci U S A, 112, E516-25.] Lipid Mediators in Health and Disease II: From The Cutting Edge • A Tribute to Edward Dennis WELCOME I would like to welcome all of the participants of the Lipid Mediators in Health and Disease II: From The Cutting Edge, A Tribute to Edward Dennis, and the 7th International Conference on Phospholipase A2 and Lipid Mediators: From Bench To Translational Medicine. This conference follows upon the very successful meeting led by Professor Jesper Z. Haeggström at the Karolinska Institutet, Nobel Forum, Stockholm, Sweden, on August 27-29, 2014, where Nobel Laureate Professor Bengt Samuelsson was honored. Lipids serve a myriad of essential functions in cell signaling, cell organization, energy metabolism, and overall homeostasis.
    [Show full text]
  • Clostridium Perfringens
    INFECTION AND IMMUNITY, Aug. 1997, p. 3485–3488 Vol. 65, No. 8 0019-9567/97/$04.0010 Copyright © 1997, American Society for Microbiology Clostridium perfringens Enterotoxin Lacks Superantigenic Activity but Induces an Interleukin-6 Response from Human Peripheral Blood Mononuclear Cells TERESA KRAKAUER,1 BERNHARD FLEISCHER,2 DENNIS L. STEVENS,3,4 5 1 BRUCE A. MCCLANE, AND BRADLEY G. STILES * Department of Immunology and Molecular Biology, U.S. Army Medical Research Institute of Infectious Diseases, Frederick, Maryland1; Bernhard Nocht Institute for Tropical Medicine, Hamburg, Germany2; Infectious Diseases Section, Veterans Administration Medical Center, Boise, Idaho3; University of Washington School of Medicine, Seattle, Washington4; and Department of Molecular Genetics and Biochemistry, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania5 Received 20 February 1997/Returned for modification 3 April 1997/Accepted 22 May 1997 We investigated the potential superantigenic properties of Clostridium perfringens enterotoxin (CPE) on human peripheral blood mononuclear cells (PBMC). In contrast to the findings of a previous report (P. Bowness, P. A. H. Moss, H. Tranter, J. I. Bell, and A. J. McMichael, J. Exp. Med. 176:893–896, 1992), two different, biologically active preparations of CPE had no mitogenic effects on PBMC. Furthermore, PBMC incubated with various concentrations of CPE did not elicit interleukin-1, interleukin-2, gamma interferon, or tumor necrosis factor alpha or beta, which are cytokines commonly associated with superantigenic stimulation. However, CPE did cause a dose-related release of interleukin-6 from PBMC cultures. Clostridium perfringens enterotoxin (CPE) is traditionally Additionally, the full-length recombinant CPE species used in recognized as a virulence factor responsible for the diarrheal this study has recently been characterized in detail (10) and and cramping symptoms associated with C.
    [Show full text]
  • Scientific Program
    Scientific Program 1 he Annual Meeting of the Brazilian Biophysics Society, one of the largest T and most traditional gathering of Biophysicists in Latin America, occurs during the second semester of each year. Now in its 43rd edition, the 2018 meeting will be held again at the Mendes Plaza Hotel, in the city of Santos (SP), from September 27th to 30th. A rich program of 16 symposia, 4 plenary talks, and 2 poster sessions covering a broad range of topics in Biophysics will guarantee the appropriate environment for productive discussions about developments regarding Biophysics and its interfaces with Biochemistry, Medicine, Pharmacy, among other disciplines. World leaders in several areas of Biophysics, from at least 12 different countries have already confirmed participation in our meeting this year! We will host researchers from Argentina, Belgium, Canada, Denmark, England, France, Germany, Israel, Portugal, United States, Uruguay and, of course, from Brazil, which will be represented by colleagues from 10 different states. This shows our broad representation in both national and international scenarios. We believe our meeting is the perfect opportunity for researchers interested in Biophysics and related fields to present their latest results to a very distinguished audience. Therefore, we invite you to participate and to submit an abstract for the poster sessions. Looking forward to seeing you in Santos! Antonio Costa-Filho President of SBBf 2 3 Index Iseli L. Nantes Cardoso ................................................ 56 Tayana Mazin Tsubone ................................................. 83 Juliana S Yoneda ........................................................ 57 Yan M. H. Gonçalves ................................................... 84 Organizing Committee ............................................7 Katia Regina Perez ....................................................... 33 Lucas Rodrigues de Mello............................................ 57 Yeny Y. P. Valencia ....................................................
    [Show full text]
  • Universidade De São Paulo Escola De Comunicações E Artes Departamento De Informação E Cultura
    UNIVERSIDADE DE SÃO PAULO ESCOLA DE COMUNICAÇÕES E ARTES DEPARTAMENTO DE INFORMAÇÃO E CULTURA Bruna Acylina Gallo Indicadores de Produção Científica: o caso do Instituto Butantan São Paulo 2019 Bruna Acylina Gallo Indicadores de Produção Científica: o caso do Instituto Butantan Relatório Final de Iniciação Científica submetido ao Departamento de Informação e Cultura da Escola de Comunicações e Artes da Universidade de São Paulo. Orientador: Profª. Drª. Nair Yumiko Kobashi São Paulo 2019 AGRADECIMENTOS Gostaria de agradecer à minha orientadora, professora Nair Yumiko Kobashi por orientar este trabalho e por tantos aprendizados. E à Mariana Crivelente por me auxiliar nessa caminhada, pela paciência e colaboração, pois o trabalho analisou parte dos dados do projeto de sua dissertação “Métodos e técnicas bibliométricas de análise de produção científica: um estudo crítico”, do Programa de Pós- Graduação em Ciência da Informação da Escola de Comunicações e Artes. RESUMO Análise de produção científica do Instituto Butantan, do período 2007-2016, recuperados na Plataforma Lattes. O objetivo da pesquisa foi compreender os conceitos e métodos da Bibliometria e realizar um estudo de caso para aplicá-los. O trabalho seguiu os seguintes procedimentos: revisão de literatura; recuperação de artigos de pesquisadores do Instituto Butantan registrados na Plataforma Lattes; limpeza e normalização dos dados; tratamento bibliométrico dos dados; comparação dos resultados com os indicadores de produção científica publicados nos relatórios anuais do Instituto Butantan. Os resultados referem-se aos seguintes aspectos: indicadores de produção científica e de outras atividades de pesquisa e discussão dos problemas encontrados na produção de indicadores. O processo de pesquisa foi importante para conhecer os conceitos e métodos da Bibliometria e trazer à luz os diversos problemas enfrentados em estudos bibliométricos.
    [Show full text]
  • Perspectives
    PERSPECTIVES not undergone decomposition failed to have TIMELINE such effects. In attempts to isolate and charac- terize the poisonous material, Peter L. Panum (1820–1885) could be considered a pioneer. Innate immune sensing and its roots: He showed that putrid fluids contained a water-soluble, but alcohol-insoluble, heat- the story of endotoxin resistant, non-volatile substance, which was lethal to dogs3. Also, Ernst von Bergmann (1836–1906) believed that a chemically Bruce Beutler and Ernst Th. Rietschel defined substance was responsible for putrid intoxication, which he termed sepsin4. How does the host sense pathogens? formed the conceptual framework within Of course, the contagionists could not Our present concepts grew directly which early workers sought to identify it. explain how a single contact with putrid flu- from longstanding efforts to understand Impressed by the malodorous exhalations ids or a sick patient could transmit so much infectious disease: how microbes harm of patients suffering from plague and their poison that not only the affected person, but the host, what molecules are sensed and, similarity to the foul vapours emanating from also thousands of other people, would die. It ultimately, the nature of the receptors that marshes, physicians came to believe that the was, therefore, an intellectual breakthrough the host uses. The discovery of the host putative poison was generated by putrefac- to postulate that the putrid venom commu- sensors — the Toll-like receptors — was tion (from the Greek for sepsis) of organic nicated by miasma or contagion could rooted in chemical, biological and genetic matter present in sick people or in locations reproduce in the affected individual, thereby analyses that centred on a bacterial poison, such as swamps.
    [Show full text]
  • Molecular Aspects of Endotoxic Reactions A
    BACTERIOLCGICAL REVIEWS, Mar. 1969, p. 72-98 Vol. 33, No. I Copyright © 1969 American Society for Microbiology Printed in U.S.A. Molecular Aspects of Endotoxic Reactions A. NOWOTNY Department of Microbiology, Temple University School of Medicine, Philadelphia, Pennsylvania 19122 INTRODUCTION............................................................ 72 CHEMICAL PROPERTIES AND CONSTITUENTS ............................ 73 BIOLOGICAL PROPERTIES ................................................. 73 Characteristic Endotoxic Reactions ............................................ 73 Sensitization and Desensitization Against Endotoxic Effects ....................... 75 Relationships Among Endotoxic Reactions ...................................... 76 Fate of Injected Endotoxins ................................................... 77 RELATION OF STRUCTURAL PARTS TO BIOLOGICAL FUNCTIONS ........ 78 Role of Polysaccharides ..................................................... 78 Role of Polypeptides ........................................................ 78 Lipid Moiety ........................................................... 78 Polysaccharide-free Endotoxic Glycolipids ....... ............................... 80 SEARCH FOR THE TOXIC PRINCIPLE ..................................... 80 Role of Hypersensitivity ..................................................... 80 Relation of Particle Size to Endotoxicity ....................................... 81 Toxic Constituents or Toxic Conformation? ..................................... 82 DETOXIFICATION AS
    [Show full text]