Relevant bibliographies by topics / Hemorrhagic toxin

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  1. Journal articles
  2. Dissertations / Theses
  3. Books
  4. Book chapters
  5. Conference papers

Academic literature on the topic 'Hemorrhagic toxin'

Author: Grafiati
Published: 4 June 2021
Last updated: 1 February 2022

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Journal articles on the topic "Hemorrhagic toxin"

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Miah, MS, M. Asaduzzaman, A. Siddika, N. Popy, MA Sufian, and MM Hossain. "Detection of Toxic Effects of Clostridial Crude Toxin in Experimental Rats." Progressive Agriculture 21, no. 1-2 (2013): 65–72. http://dx.doi.org/10.3329/pa.v21i1-2.16753.

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The present study was conducted for the detection of toxic effects of clostridial crude toxin in experimental rats. The crude toxin of Clostridium perfringens was prepared and the rats were injected intraperitoneally (IP) 0.5 ml, 1.0 ml and 2.0 ml of crude toxin. The rats were observed for 24 hrs. The crude toxin inoculated rats showed the dose dependent clinical signs; depression, rough hair coat, respiratory distress, diarrhea and rapid heart beats, whereas PBS inoculated rats did not show any clinical sings. Necropsy changes were variable however, highly dilated and distended whole intestin
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Jacewicz, Mary S., David W. K. Acheson, David G. Binion, et al. "Responses of Human Intestinal Microvascular Endothelial Cells to Shiga Toxins 1 and 2 and Pathogenesis of Hemorrhagic Colitis." Infection and Immunity 67, no. 3 (1999): 1439–44. http://dx.doi.org/10.1128/iai.67.3.1439-1444.1999.

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ABSTRACT Endothelial damage is characteristic of infection with Shiga toxin (Stx)-producing Escherichia coli (STEC). Because Stx-mediated endothelial cell damage at the site of infection may lead to the characteristic hemorrhagic colitis of STEC infection, we compared the effects of Stx1 and Stx2 on primary and transformed human intestinal microvascular endothelial cells (HIMEC) to those on macrovascular endothelial cells from human saphenous vein (HSVEC). Adhesion molecule, interleukin-8 (IL-8), and Stx receptor expression, the effects of cytokine activation and Stx toxins on these responses,
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Genth, Harald, Fred Hofmann, Jörg Selzer, Gundula Rex, Klaus Aktories, and Ingo Just. "Difference in Protein Substrate Specificity between Hemorrhagic Toxin and Lethal Toxin fromClostridium sordellii." Biochemical and Biophysical Research Communications 229, no. 2 (1996): 370–74. http://dx.doi.org/10.1006/bbrc.1996.1812.

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Moxley, Rodney A. "Special Issue: Shiga Toxin-Producing Escherichia coli." Microorganisms 9, no. 1 (2020): 1. http://dx.doi.org/10.3390/microorganisms9010001.

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Globally, Shiga toxin-producing Escherichia coli (STEC) is an important cause of diarrheal disease, most notably hemorrhagic colitis, and post-diarrheal sequela, such as hemolytic-uremic syndrome (HUS) [...]
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Lukyanenko, Valeriy, Irina Malyukova, Ann Hubbard, et al. "EnterohemorrhagicEscherichia coliinfection stimulates Shiga toxin 1 macropinocytosis and transcytosis across intestinal epithelial cells." American Journal of Physiology-Cell Physiology 301, no. 5 (2011): C1140—C1149. http://dx.doi.org/10.1152/ajpcell.00036.2011.

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Gastrointestinal infection with Shiga toxins producing enterohemorrhagic Escherichia coli causes the spectrum of gastrointestinal and systemic complications, including hemorrhagic colitis and hemolytic uremic syndrome, which is fatal in ∼10% of patients. However, the molecular mechanisms of Stx endocytosis by enterocytes and the toxins cross the intestinal epithelium are largely uncharacterized. We have studied Shiga toxin 1 entry into enterohemorrhagic E. coli-infected intestinal epithelial cells and found that bacteria stimulate Shiga toxin 1 macropinocytosis through actin remodeling. This e
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Dabholkar, A. S., and W. W. Carmichael. "Ultrastructural changes in the mouse liver induced by hepatotoxin from the freshwater cyanobacterium Microcystis aeruginosa." Proceedings, annual meeting, Electron Microscopy Society of America 44 (August 1986): 360–61. http://dx.doi.org/10.1017/s0424820100143420.

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The colonial cyanobacterium (Blue-green alga) Microcystis aeruginosa can form heavy growths or waterblooms of toxic cells in drinking and recreational water supplies. Intraperitoneal (i.p.) administration of toxic cells (LD50 i.p. mouse = 40 mg/kg) or purified toxin (50 μg/kg) causes death in laboratory rats or mice within 1-3 h. The most acutely affected organ is the liver which shows severe hemorrhagic necrosis. Previous liver ultrastructure studies have shown damaged endothelium, swollen mitochondria and fragmented membranes. Our time-course electron microscopic study is focused on the time
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da Silva, W. Dias, L. R. C. Gonçalves, A. C. M. R. Campos, et al. "Experimental antivenom to a caterpillar toxin inducing hemorrhagic disorder." Toxicon 33, no. 3 (1995): 262. http://dx.doi.org/10.1016/0041-0101(95)99248-2.

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Mehdizadeh Gohari, Iman, Stefan Unterer, Ashley E. Whitehead, and John F. Prescott. "NetF-producing Clostridium perfringens and its associated diseases in dogs and foals." Journal of Veterinary Diagnostic Investigation 32, no. 2 (2020): 230–38. http://dx.doi.org/10.1177/1040638720904714.

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The role of type A Clostridium perfringens in canine acute hemorrhagic diarrhea syndrome and foal necrotizing enteritis is poorly characterized. However, a highly significant association between the presence of novel toxigenic C. perfringens and these specific enteric diseases has been described. These novel toxigenic strains produce 3 novel putative toxins, which have been designated NetE, NetF, and NetG. Although not conclusively demonstrated, current evidence suggests that NetF is likely the major virulence factor in strains responsible for canine acute hemorrhagic diarrhea syndrome and foa
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Genth, Harald, Jörg Selzer, Christian Busch, et al. "New Method To Generate Enzymatically DeficientClostridium difficile Toxin B as an Antigen for Immunization." Infection and Immunity 68, no. 3 (2000): 1094–101. http://dx.doi.org/10.1128/iai.68.3.1094-1101.2000.

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ABSTRACT The family of the large clostridial cytotoxins, encompassingClostridium difficile toxins A and B as well as the lethal and hemorrhagic toxins from Clostridium sordellii, monoglucosylate the Rho GTPases by transferring a glucose moiety from the cosubstrate UDP-glucose. Here we present a new detoxification procedure to block the enzyme activity by treatment with the reactive UDP-2′,3′-dialdehyde to result in alkylation of toxin A and B. Alkylation is likely to occur in the catalytic domain, because the native cosubstrate UDP-glucose completely protected the toxins from inactivation and
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Svetoch, E. A., I. A. Dyatlov, N. N. Kartsev, B. V. Eruslanov, M. E. Kanashenko, and N. K. Fursova. "Development of candidate vaccines against infection caused by shiga-toxin producing Escherichia coli. Part 1." Bacteriology 5, no. 2 (2020): 56–70. http://dx.doi.org/10.20953/2500-1027-2020-2-56-70.

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Shiga-toxin producing Escherichia coli (STEC) strains cause serious and life-threatening diseases, hemorrhagic colitis (HC) and associated hemolytic uremic syndrome (HUS). Antibacterial etiotropic therapy against these diseases are not recommended. There are no vaccines against human HA and HUS. The review provides materials on the design of various types of candidate vaccines against STEC strains and assessment of their immunogenic and protective properties in experiments on laboratory and farm animals. The prospects for the use of inactivated corpuscular and live (vector) vaccines, lipopolys
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Dissertations / Theses on the topic "Hemorrhagic toxin"

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Fogo, Verônica Simões. "Prevalência e caracterização de Escherichia coli O157:H7 e outras cepas produtoras de toxina de Shiga (STEC) na linha de abate de carne bovina destinada à exportação." Universidade de São Paulo, 2009. http://www.teses.usp.br/teses/disponiveis/9/9131/tde-27012017-123850/.

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Escherichia coli é um microrganismo presente no trato intestinal do homem e de animais de sangue quente, fazendo parte da microbiota, coexistindo sem causar danos ao hospedeiro. No entanto, algumas linhagens desse microrganismo podem ser patogênicas e causar doenças tanto ao homem como aos animais. E. coli produtoras de toxina de Shiga (STEC), consideradas patógenos de origem alimentar, podem causar desde diarréias brandas até severas e sanguinolentas a complicações graves, como colite hemorrágica (HC), síndrome urêmica hemolítica (HUS) e púrpura trombótica trombocitopênica (TTP). O gado é con
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Ebrahimian, Venus. ""Characterization of Red Diamondback Rattlesnake Venom Proteins on Cell Death and Function"." Wright State University / OhioLINK, 2013. http://rave.ohiolink.edu/etdc/view?acc_num=wright1389638004.

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Dennis, Patricia Marie. "Epidemiology of black rhinoceroses (Diceros bicornis) in captivity in the United States." Connect to this title online, 2004. http://rave.ohiolink.edu/etdc/view?acc%5Fnum=osu1095785660.

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Thesis (Ph. D.)--Ohio State University, 2004.<br>Document formatted into pages; contains xiii, 126 p. Includes bibliographical references. Abstract available online via OhioLINK's ETD Center; full text release delayed at author's request until 2007 Sept. 21.
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Nowell, Victoria. "GENOMIC AND PROTEOMIC ANALYSIS OF A BOVINE HEMORRHAGIC ABOMASITIS TYPE A CLOSTRIDIUM PERFRINGENS ISOLATE." Thesis, 2011. http://hdl.handle.net/10214/2982.

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This study sought to understand the pathogenesis of hemorrhagic abomasitis in calves by characterizing a type A Clostridium perfringens isolate. The complete genome sequence of an isolate from an outbreak of hemorrhagic abomasitis was compared to the three complete C. perfringens genomes currently available in GenBank. Unique findings included the presence of an integrated plasmid sequence and a frameshift mutation in the virS gene, which encodes the main sensor kinase that controls virulence gene regulation. An ~ 55 kb plasmid similar to pCW3 was found, in addition to two smaller plasmids wit
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Henriques, Patrícia Ferreira Dias. "Relatórios de Estágio e Monografia intitulada “Influence of ABC-efflux transporters on the toxic effects of the direct oral anticoagulant drugs”." Master's thesis, 2018. http://hdl.handle.net/10316/84421.

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Relatório de Estágio do Mestrado Integrado em Ciências Farmacêuticas apresentado à Faculdade de Farmácia<br>No âmbito da unidade curricular de Estágio Curricular do Mestrado Integrado em Ciências Farmacêuticas da Faculdade de Farmácia da Universidade de Coimbra, o presente documento apresenta, sob a forma de uma análise SWOT, o relatório de estágio em Farmácia Comunitária, realizado na Farmácia do Fórum, e o relatório de estágio na Direção de Avaliação de Medicamentos do INFARMED - Autoridade Nacional do Medicamento e Produtos de Saúde, I. P. Este documento inclui ainda a monografia intitulada
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Books on the topic "Hemorrhagic toxin"

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Rice, Anne. Lasher. Libro Express, 1997.

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Rice, Anne. Lasher. 8th ed. Penguin Books, 1994.

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Rice, Anne. Lasher. Ballantine Books, 1994.

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Rice, Anne. Lasher. Alfred A. Knopf, 1993.

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Rice, Anne. L'heure des sorcieres: Roman. Robert Laffont, 1998.

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Rice, Anne. Lasher. Chatto & Windus, 1993.

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Rice, Anne. Lasher. Alfred A. Knopf, 1993.

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Rice, Anne. Lasher. Ballantine Books, 1995.

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Rice, Anne. Lasher: Lives of the Mayfair Witches. Ballantine Books, 1995.

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Rice, Anne. Il Demone Incarnato: Romanzo. TEA, 2006.

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Book chapters on the topic "Hemorrhagic toxin"

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Ownby, Charlotte L. "Pathogenesis of Hemorrhage Induced by Rattlesnake Venoms and Their Purified Hemorrhagic Toxins." In Vascular Endothelium. Springer US, 1991. http://dx.doi.org/10.1007/978-1-4615-3736-6_50.

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Anderson, Steffan G., and Charlott L. Ownby. "Isolation of an 86 KDa Hemorrhagic Toxin from the Venom of the Eastern Diamondback Rattlesnake (Crotalus Adamanteus) and its Effect of Rat Aorta Endothelial Cells in Culture." In Vascular Endothelium. Springer US, 1996. http://dx.doi.org/10.1007/978-1-4613-0355-8_16.

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žek, Daniel, Michael Holbrook, Valeriy Yakimenko, Lyudmila Karan, and Sergey Tkachev. "Omsk Hemorrhagic Fever Virus." In Manual of Security Sensitive Microbes and Toxins. CRC Press, 2014. http://dx.doi.org/10.1201/b16752-19.

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Puerta-Guardo, Henry, Scott B. Biering, Eva Harris, et al. "Dengue Immunopathogenesis: A Crosstalk between Host and Viral Factors Leading to Disease: Part I - Dengue Virus Tropism, Host Innate Immune Responses, and Subversion of Antiviral Responses." In Dengue Fever in a One Health Perspective. IntechOpen, 2020. http://dx.doi.org/10.5772/intechopen.93140.

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Dengue is the most prevalent emerging mosquito-borne viral disease, affecting more than 40% of the human population worldwide. Many symptomatic dengue virus (DENV) infections result in a relatively benign disease course known as dengue fever (DF). However, a small proportion of patients develop severe clinical manifestations, englobed in two main categories known as dengue hemorrhagic fever (DHF) and dengue shock syndrome (DSS). Secondary infection with any of the four dengue virus serotypes (DENV1, -2, -3, and -4) is a risk factor to develop severe forms of dengue disease. DSS is primarily characterized by sudden and abrupt endothelial dysfunction, resulting in vascular leak and organ impairment, which may progress to hypovolemic shock and death. Severe DENV disease (DHF/DSS) is thought to follow a complex relationship between distinct immunopathogenic processes involving host and viral factors, such as the serotype cross-reactive antibody-dependent enhancement (ADE), the activation of T cells and complement pathways, the phenomenon of the cytokine storm, and the newly described viral toxin activity of the nonstructural protein 1 (NS1), which together play critical roles in inducing vascular leak and virus pathogenesis. In this chapter that is divided in two parts, we will outline the recent advances in our understanding of DENV pathogenesis, highlighting key viral-host interactions and discussing how these interactions may contribute to DENV immunopathology and the development of vascular leak, a hallmark of severe dengue. Part I will address the general features of the DENV complex, including the virus structure and genome, epidemiology, and clinical outcomes, followed by an updated review of the literature describing the host innate immune strategies as well as the viral mechanisms acting against and in favor of the DENV replication cycle and infection.
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Erbay, Ayse. "Crimean-Congo Hemorrhagic Fever Virus." In Manual of Security Sensitive Microbes and Toxins. CRC Press, 2014. http://dx.doi.org/10.1201/b16752-7.

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"Alveolar Hemorrhage Related to Drugs/Toxins." In Thurlbeck's Pathology of the Lung, edited by Andrew M. Churg, Jeffrey L. Myers, Henry D. Tazelaar, and Joanne L. Wright. Georg Thieme Verlag, 2005. http://dx.doi.org/10.1055/b-0034-77271.

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Tu, Anthony T. "Tissue Damaging Effects by Snake Venoms: Hemorrhage and Myonecrosis." In Handbook of Natural Toxins. Routledge, 2018. http://dx.doi.org/10.1201/9780203752715-11.

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Ownby, Charlotte L. "Locally Acting Agents: Myotoxins, Hemorrhagic Toxins and Dermonecrotic Factors." In Handbook of Toxinology. CRC Press, 2020. http://dx.doi.org/10.1201/9781003066538-8.

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Razin, Assaf. "The 2008 Global Crisis and Israel-Economy Resilience." In Israel and the World Economy. The MIT Press, 2018. http://dx.doi.org/10.7551/mitpress/9780262037341.003.0005.

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The global financial crisis generated the deepest and longest recession since the Great Depression of the 1930s. The defining event of the 2008 global financial crisis was a “hemorrhagic stroke”: a paralytic implosion of the loanable funds markets. Depression forces such as they exist in the US, Europe, or Japan, do not appear to hold in the case of Israel. Its resilience to the external financial shock during the global crisis is rooted in (a) the absence of credit boom in the wake of the crisis, and (b) the relatively small commercial banks' exposure in terms of toxic assets that for the European countries played a major role. Reacting to the global trade-diminishing shocks, policy makers’ concern was three-fold: First, banks exposures to toxic assets such as mortgage based securities and foreigners’ debt obligations. Partly because Israel skipped the credit bubble, and bank regulations were relatively tight, Israel showed a sound resilience to the global financial shock. Second, Israel export markets softened and demand conditions deteriorated. Third, Israel domestic currency got strengthened. Bank of Israel addressed the last two issues by a massive foreign exchange market intervention to weaken the value of the domestic currency, and stimulate exports. The need to prolong the stimulus policies dissipated relatively fast.
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Orr, David W. "A Politics Worthy of the Name." In The Nature of Design. Oxford University Press, 2002. http://dx.doi.org/10.1093/oso/9780195148558.003.0018.

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Relative to the problems we face, our politics are about the most miserable that can be imagined. Those who purport to represent us and who on rare occasions try to lead us have been unable to take even the smallest steps to promote energy efficiency to avoid possibly catastrophic climatic change a few decades from now. They have failed to stop the hemorrhaging of life and protect biological diversity, soils, and forests. They ignore problems of urban decay, suburban sprawl, the poisoning of our children by persistent toxins, the destruction of rural communities, and the growing disparity between the rich and the poor. They cannot find the wherewithal to defend the public interest in matters of global trade or even in the financing of public elections. Indeed, the more potentially catastrophic the issue, the less likely it is to receive serious and sustained attention from political leaders at any level. Our public priorities, in other words, are upside down. Issues that will seem trivial or even nonsensical to our progeny are given great attention, while problems crucial to their well-being are ignored and allowed to grow into global catastrophes. At best they will regard us with pity, at worst as derelict and perhaps criminally so. The situation was not always this way. The leadership of this country was once capable of responding to threats to our security and health with alacrity and sometimes with intelligence. In light of the dismal performance of the U.S. political system relative to the large environmental and social issues looming ahead, we have, broadly speaking, three possible courses of action (assuming that we choose to act). The first is to turn the management of our environmental affairs over to a kind of permanent technocracy—a priesthood of global managers. The idea that experts ought to manage public affairs is at least as old as Plato. In its current incarnation, some propose to turn the management of the earth over to a group of global experts. Stripped to its essentials, this means smarter exploitation of nature culminating in the global administration of the planet with lots of satellites, remote sensing, and geographic information systems experts mapping one thing or another.
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Conference papers on the topic "Hemorrhagic toxin"

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Gentry, P. A., and G. S. Bondy. "The aggregation of bovine platelets is not dependent on thromboxane B2 production." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644500.

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Bovine and human platelets appear to be equally sensitive to inhibition by several environmental toxins even though the bovine is not generally recognised as a species prone to thromboembolic and hemorrhagic disease. During the examination of the mechanism of action of the toxins it became necessary to establish parameters for normal bovine platelet function.Bovine platelets suspended in homologous plasma demonstrate various responses to different agonists. Bovine platelets aggregate effectively and irreversibly to fibrillar form collagen and adenosine-diphosphate (ADP), undergo reversible agg
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