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Relevant bibliographies by topics / Alpha toxin

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Academic literature on the topic 'Alpha toxin'

Author: Grafiati

Published: 4 June 2021

Last updated: 7 February 2022

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Journal articles on the topic "Alpha toxin"

1

Liang, Xudong, Meiying Yan, and Yinduo Ji. "The H35A Mutated Alpha-Toxin Interferes with Cytotoxicity of Staphylococcal Alpha-Toxin." Infection and Immunity 77, no. 3 (December 22, 2008): 977–83. http://dx.doi.org/10.1128/iai.00920-08.

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ABSTRACT Staphylococcal alpha-toxin is an important virulence factor for Staphylococcus aureus to cause severe infections. In this study, we explored whether the toxoid of alpha-toxin may be utilized to block the toxicity of wild-type alpha-toxin. We created a series of H35A mutated alpha-toxin expression strains and revealed that the H35A mutation eliminates the activity of alpha-toxin using a human lung epithelial cell line (A549). More importantly, we found that either the pretreatment or simultaneous treatment of the epithelial cells with alpha-toxin-H35A completely disrupted the cytotoxicity of alpha-toxin. Specifically, we demonstrated that alpha-toxin-H35A can effectively interfere with the pore formation and the internalization of alpha-toxin using cytotoxicity and immunofluorescence assays. In addition, we found that the removal of either the 30-amino-acid (aa) or 99-aa C-terminal region of alpha-toxin-H35A reactivated its cytotoxicity, indicating that interactions between the alanine residue at position 35 and these C-terminal regions may be associated with interrupting the toxic activity of alpha-toxin-H35A. Taken together, these results suggest that the alpha-toxin-H35A protein may be developed as a potential alternative therapeutic agent for treating early stages of S. aureus infections.

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Bernheimer, Alan W. "STAPHYLOCOCCAL ALPHA TOXIN*." Annals of the New York Academy of Sciences 128, no. 1 (December 16, 2006): 112–23. http://dx.doi.org/10.1111/j.1749-6632.1965.tb11633.x.

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3

Palmer. "Staphyloccal alpha toxin." Journal of Applied Microbiology 84, S1 (July 1998): 125S—126S. http://dx.doi.org/10.1046/j.1365-2672.1998.0840s1125s.x.

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4

Jepson, Marie, Angela Howells, Helen L. Bullifent, Barbara Bolgiano, Dennis Crane, Julie Miller, Jane Holley, Pramukh Jayasekera, and Richard W. Titball. "Differences in the Carboxy-Terminal (Putative Phospholipid Binding) Domains of Clostridium perfringens andClostridium bifermentans Phospholipases C Influence the Hemolytic and Lethal Properties of These Enzymes." Infection and Immunity 67, no. 7 (July 1, 1999): 3297–301. http://dx.doi.org/10.1128/iai.67.7.3297-3301.1999.

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ABSTRACT The phospholipases C of C. perfringens (alpha-toxin) and C. bifermentans (Cbp) show >50% amino acid homology but differ in their hemolytic and toxic properties. We report here the purification and characterisation of alpha-toxin and Cbp. The phospholipase C activity of alpha-toxin and Cbp was similar when tested with phosphatidylcholine in egg yolk or in liposomes. However, the hemolytic activity of alpha-toxin was more than 100-fold that of Cbp. To investigate whether differences in the carboxy-terminal domains of these proteins were responsible for differences in the hemolytic and toxic properties, a hybrid protein (NbiCα) was constructed comprising the N domain of Cbp and the C domain of alpha-toxin. The hemolytic activity of NbiCαwas 10-fold that of Cbp, and the hybrid enzyme was toxic. These results confirm that the C-terminal domain of these proteins confers different properties on the enzymatically active N-terminal domain of these proteins.

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Zhu, H., and H. Bussey. "Mutational analysis of the functional domains of yeast K1 killer toxin." Molecular and Cellular Biology 11, no. 1 (January 1991): 175–81. http://dx.doi.org/10.1128/mcb.11.1.175.

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To determine the functional domains of K1 killer toxin, we analyzed the phenotypes of a set of mutations throughout regions encoding the alpha- and beta-toxin subunits that allow secretion of mutant toxins. A range of techniques have been used to examine the ability of mutant toxins to bind to beta-glucan cell wall receptor and to form lethal ion channels. Our results indicate that both the alpha and beta subunits are involved in beta-glucan receptor binding. Defects in ion channel formation and toxin immunity are confined to the hydrophobic alpha subunit of the toxin.

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Zhu, H., and H. Bussey. "Mutational analysis of the functional domains of yeast K1 killer toxin." Molecular and Cellular Biology 11, no. 1 (January 1991): 175–81. http://dx.doi.org/10.1128/mcb.11.1.175-181.1991.

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To determine the functional domains of K1 killer toxin, we analyzed the phenotypes of a set of mutations throughout regions encoding the alpha- and beta-toxin subunits that allow secretion of mutant toxins. A range of techniques have been used to examine the ability of mutant toxins to bind to beta-glucan cell wall receptor and to form lethal ion channels. Our results indicate that both the alpha and beta subunits are involved in beta-glucan receptor binding. Defects in ion channel formation and toxin immunity are confined to the hydrophobic alpha subunit of the toxin.

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Yarovinsky, Timur O., Martha M. Monick, Matthias Husmann, and Gary W. Hunninghake. "Interferons Increase Cell Resistance to Staphylococcal Alpha-Toxin." Infection and Immunity 76, no. 2 (December 10, 2007): 571–77. http://dx.doi.org/10.1128/iai.01088-07.

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ABSTRACT Many bacterial pathogens, including Staphylococcus aureus, use a variety of pore-forming toxins as important virulence factors. Staphylococcal alpha-toxin, a prototype β-barrel pore-forming toxin, triggers the release of proinflammatory mediators and induces primarily necrotic death in susceptible cells. However, whether host factors released in response to staphylococcal infections may increase cell resistance to alpha-toxin is not known. Here we show that prior exposure to interferons (IFNs) prevents alpha-toxin-induced membrane permeabilization, the depletion of ATP, and cell death. Moreover, pretreatment with IFN-α decreases alpha-toxin-induced secretion of interleukin 1β (IL-1β). IFN-α, IFN-β, and IFN-γ specifically protect cells from alpha-toxin, whereas tumor necrosis factor alpha (TNF-α), IL-6, and IL-4 have no effects. Furthermore, we show that IFN-α-induced protection from alpha-toxin is not dependent on caspase-1 or mitogen-activated protein kinases, but requires protein synthesis and fatty acid synthase activity. Our results demonstrate that IFNs may increase cell resistance to staphylococcal alpha-toxin via the regulation of lipid metabolism and suggest that interferons play a protective role during staphylococcal infections.

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TSIOURIS (Β.Σ. ΤΣΙΟΥΡΗΣ), V. S., I. GEORGOPOULOU (ΓΕΩΡΓΟΠΟΥΛΟΥ), and E. PETRIDOU (Ε. ΠΕΤΡΙΔΟΥ). "Update on the toxins of Clostridium perfringens and their actions." Journal of the Hellenic Veterinary Medical Society 61, no. 3 (November 17, 2017): 241. http://dx.doi.org/10.12681/jhvms.14892.

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Clostridia appeared as a distinct class, approximately 2.7 billion years ago, before the initial formation of oxygen. Clostridium perfringens is widely distributed throughout the environment due to its ability to form spores. Furthermore, it is a member of intestinal microbiota in animals and human. In 2002, the complete genome of C perfringens strain 13 was published. Genomic analysis has revealed that C. perfringens lacks the genetic machinery to produce 13 essential amino acids and it obtains these in vivo via the action of its toxins. Toxins of C perfringens can be divided into major, minor and enterotoxin. C perfringens strains are classified into five toxinotypes (A, B, C, D and E), based on the production of four major toxins. Alpha toxin is the best and most studied major toxin of C perfringens and it was the first bacterial toxin established to possess enzymatic activity. It has haemolytic, necrotic and cytolytic activity, it can lyse platelets and leukocytes and it can damage fibroblasts and muscle cell membranes. Expression of epa gene, which is responsible for the production of alpha toxin by C perfringens, is down-regulated in the normal healthy gut, but it is upregulated to initiate enteric disease in response to an environmental signal. C perfringens appears to be regulated in a quorum sensing manner, using oligopeptides, AI-2 or both, to regulate expression of the epa gene, and thus the synthesis of alpha toxin. Beta toxin is recognized as an important agent in necrotic enteritis of humans and it is the second most lethal C. perfringens toxin following epsilon toxin. Beta toxin is a membrane spanning protein that oligomerizes to form channels in susceptible cells or it primarily acts as a neurotoxin. Epsilon toxin is the most potent of the C. perfringens toxins and the third most potent neurotoxin from the Clostridium spp., following botulinum and tetanus toxins. Epsilon toxin of C perfringens type D causes enterotoxaemia and pulpy kidneys disease of lambs. Iota toxin causes disruption of the actin cytoskeleton and cell barrier integrity and it is the less toxic of the major toxins of C perfringens. Although C perfringens enterotoxin is not classified as one of the major toxins of C perfringens, it is the third most common cause of food poisoning in industrialized nations. It is not secreted by the cells of growing bacteria, but it is released only with the sporulation of C perfringens. Not all strains of C perfringens carry the epe gene, which is responsible for the production of enterotoxin. Theta toxin is a pore-forming cytolysin that can lyse red blood cells. It is produced by all types of C perfringens. Together with alpha-toxin, theta-toxin modulates the host inflammatory response. ß2 toxin is a pore forming toxin which is involved in necrotic enteritis of swine and horse, in haemorragic enteritis of bovine in diarrhea cases of dogs and along with enterotoxin in diarrhea cases of humans. Recently, -NetB, a novel toxin that is associated with broiler necrotic enteritis, has been described. The mechanism of its action seems to involve the formation of small hydrophilic pores. Other toxins of C. perfringens include λ-toxin, ô-toxin, μ-toxin, v-toxin, κ-toxin, a-clostripain like protease and neuraminidase/sialidase. These toxins can act as enzymes, while many of them can act synergically or supplementally with major pore forming toxins. Potentially, C. perfringens might produce more toxins, which have not been identified. Finally, the actions of C. perfringens toxins, major or minor, in some diseases have not been figured out.

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Nilsson, Ing-Marie, Orla Hartford, Timothy Foster, and Andrzej Tarkowski. "Alpha-Toxin and Gamma-Toxin Jointly PromoteStaphylococcus aureus Virulence in Murine Septic Arthritis." Infection and Immunity 67, no. 3 (March 1, 1999): 1045–49. http://dx.doi.org/10.1128/iai.67.3.1045-1049.1999.

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ABSTRACT Septic arthritis is a common and feared complication of staphylococcal infections. Staphylococcus aureus produces a number of potential virulence factors including certain adhesins and enterotoxins. In this study we have assessed the roles of cytolytic toxins in the development of septic arthritis by inoculating mice withS. aureus wild-type strain 8325-4 or isogenic mutants differing in the expression of alpha-, beta-, and gamma-toxin production patterns. Mice inoculated with either an alpha- or beta-toxin mutant showed degrees of inflammation, joint damage, and weight decrease similar to wild-type-inoculated mice. In contrast, mice inoculated with either double (alpha- and gamma-toxin-deficient)- or triple (alpha-, beta-, and gamma-toxin-deficient)-mutant S. aureus strains showed lower frequency and severity of arthritis, measured both clinically and histologically, than mice inoculated with the wild-type strain. We conclude that simultaneous production of alpha- and gamma-toxin is a virulence factor in S. aureusarthritis.

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Awad, Milena M., Darren M. Ellemor, Richard L. Boyd, John J. Emmins, and Julian I. Rood. "Synergistic Effects of Alpha-Toxin and Perfringolysin O in Clostridium perfringens-Mediated Gas Gangrene." Infection and Immunity 69, no. 12 (December 1, 2001): 7904–10. http://dx.doi.org/10.1128/iai.69.12.7904-7910.2001.

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ABSTRACT To examine the synergistic effects of alpha-toxin and perfringolysin O in clostridial myonecrosis, homologous recombination was used to construct an alpha-toxin deficient derivative of a perfringolysin O mutant of Clostridium perfringens. The subsequent strain was complemented with separate plasmids that carried the alpha-toxin structural gene (plc), the perfringolysin O gene (pfoA), or both toxin genes, and the resultant isogenic strains were examined in a mouse myonecrosis model. Synergistic effects were clearly observed in these experiments. Infection with the control strain, which did not produce either toxin, resulted in very minimal gross pathological changes, whereas the isogenic strain that was reconstituted for both toxins produced a pathology that was clearly more severe than when alpha-toxin alone was reconstituted. These changes were most apparent in the rapid spread of the disease, the gross pathology of the footpad and in the rate at which the mice had to be euthanatized for ethical reasons. Elimination of both alpha-toxin and perfringolysin O production removed most of the histopathological features typical of clostridial myonecrosis. These effects were restored when the mutant was complemented with the alpha-toxin structural gene, but reconstituting only perfringolysin O activity produced vastly different results, with regions of coagulative necrosis, apparently enhanced by vascular disruption, being observed. Reconstitution of both alpha-toxin and perfringolysin O activity produced histopathology most similar to that observed with the alpha-toxin reconstituted strain. The spreading of myonecrosis was very rapid in these tissues, and coagulative necrosis appeared to be restricted to the lumen of the blood vessels. The results of these virulence experiments clearly support the hypothesis that alpha-toxin and perfringolysin O have a synergistic effect in the pathology of gas gangrene.

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Dissertations / Theses on the topic "Alpha toxin"

1

Guttenberg, Gregor [Verfasser], and Manfred [Akademischer Betreuer] Jung. "Clostridiale Glukosylierende Toxine: Untersuchungen zur Autoprozessierung von Clostridium sordellii Letalem Toxin und Clostridium novyi alpha-Toxin sowie funktionelle Charakterisierung von Clostridium perfringens TpeL-Toxin." Freiburg : Universität, 2012. http://d-nb.info/1123467994/34.

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Eaton, Julian Timothy. "Structural studies of Clostridium perfringens alpha toxin." Thesis, Birkbeck (University of London), 2003. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.417896.

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Justin, Neil. "Structural studies of clostridium perfringens alpha toxin." Thesis, Birkbeck (University of London), 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.392355.

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Reutemann, Mathias. "ICAM-1 abhängige Akkumulation neutrophiler Granulozyten und Leukotrien-vermittelte Kardiodepression in Staphylococcus aureus [alpha]-Toxin-perfundierten [Alpha-Toxin-perfundierten] Rattenherzen." [S.l.] : [s.n.], 2002. http://deposit.ddb.de/cgi-bin/dokserv?idn=965811611.

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Carnegie, Andrew Mark. "Effects of C.perfringens alpha toxin on cell signalling." Thesis, Birkbeck (University of London), 2004. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.416052.

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Wegner, Judith. "Exotoxin-Schock, ausgelöst durch Staphylococcus-aureus-[alpha]-Toxin [Staphylococcus-aureus-alpha-Toxin], am Tiermodell Ratte Auswirkungen auf Gefässendothel, Leukozytenakkumulation und Thrombozytenaggregation /." [S.l.] : [s.n.], 2005. http://deposit.ddb.de/cgi-bin/dokserv?idn=97606538X.

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Sawicki, Maria. "Immunological studies on staphylococcal alpha toxin and its fragments." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1999. http://www.collectionscanada.ca/obj/s4/f2/dsk1/tape7/PQDD_0020/MQ52656.pdf.

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Penha, Marcelo De Luca. "Detecção dos genes das toxinas alfa, beta e épsilon de Clostridium perfringens isolados a partir de amostras clínicas de bovinos pela reação em cadeia da polimerase." Universidade de São Paulo, 2004. http://www.teses.usp.br/teses/disponiveis/10/10134/tde-06072005-101119/.

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O Clostridium perfringens é um microrganismo anaeróbio que está presente no solo e no trato intestinal dos mamíferos. Provoca intoxicação alimentar nos seres humanos, doenças enterotoxêmicas nos animais domésticos e gangrena gasosa em ambos os grupos. O C. perfringens é classificado em cinco tipos (A, B, C, D e E) mediante a produção de quatro toxinas principais (alfa, beta, épsilon e iota). Neste trabalho foi possível padronizar a técnica de PCR para detectar a presença dos genes cpa, cpb e etx a partir de culturas de C. perfringens. A sensibilidade analítica da técnica de PCR a partir de culturas de C. perfringens foi de 2,27 ng/µL para o gene cpa, 22,7 pg/µL para o gene cpb e 22,7 pg/µL para o gene etx. A pesquisa dos genes cpa, cpb e etx partir de 35 amostras de C. perfringens isoladas de bovinos revelou que 16 (45,7%) eram do tipo A; 18 (51,4%) eram do tipo C e 1 (2,9%) era do tipo B. Não foi observada nenhuma amostra do tipo D. A metodologia de PCR revelou-se útil na tipificação de amostras de C. perfringens isoladas de bovinos, contribuindo para o diagnóstico dessa bacteriose neste país, eliminando as dificuldades de tipificação oriundas do alto custo e da indisponibilidade de anti-soros para a tipificação pela reação de soroneutralização e evitando a utilização de animais de laboratório.
Clostridium perfringens is an anaerobic micro-organism that is present in the soil and gastrointestinal tract of mammals. It causes food poisoning in humans, enterotoxemic diseases in domestic animals and gas gangrene in both. C. perfringens is classified into five types (A, B, C, D and E) according to the production of four major toxins (alpha, beta, epsilon and iota). In this trial was possible to standardize the PCR?s technique to detect cpa, cpb and etx genes from cultures of C. perfringens. PCR?s analythical sensibility was 2.27 ng/µL for cpa gene, 22.7 pg/µL for cpb gene and 22.7 pg/µL for etx gene. The research of cpa, cpb and etx genes from 35 samples of C. perfringens isolated from cattle reveals that 16 (45.7%) were classified as type A, 18 (51.4%) as type C and 1 (2.9%) as type B. No sample of type D was observed. PCR?s technique reveals to be usefull to typify samples of C. perfringens isolated from cattle, contributing to diagnose of this bacterial disease in this country and solving typifing problems represented by the high costs of the process and by the lack of antiserum that is required to typify the micro-organism by seroneutralization. PCR?s technique avoid the use of laboratory animals, too.

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Leslie, Dario Lyall. "Genetic analysis of alpha toxin (phospholipase C) from Clostridium perfringens." Thesis, University of Newcastle Upon Tyne, 1989. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.346420.

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Sylvester, Ian David. "The characterisation and conjugation of the fungal toxin #alpha#-sarcin." Thesis, University of Warwick, 1995. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.308083.

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Books on the topic "Alpha toxin"

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Sylvester, Ian David. The characterisation and conjugation of the fungal toxin [alpha]-sarcin. [s.l.]: typescript, 1995.

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2

International Conference on Tumor Necrosis Factor and Related Cytokines (4th 1992 Veldhoven, Netherlands). Tumor necrosis factor: Molecular and cellular biology and clinical relevance. Edited by Fiers Walter and Buurman Wim A. Basel: Karger, 1993.

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3

Mechanical stimulation of skeletal muscle increases prostaglandin F[alpha] synthesis and cyclooxygenase activity by a pertussis toxin sensitive mechanism. Providence, RI: Dept. of Pathology and Laboratory Medicine, Brown University School of Medicine and the Miriam Hospital, 1992.

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4

H, Vandenburgh Herman, and United States. National Aeronautics and Space Administration., eds. Mechanical stimulation of skeletal muscle increases prostaglandin F[́alpha] synthesis and cyclooxygenase activity by a pertussis toxin sensitive mechanism. Providence, RI: Dept. of Pathology and Laboratory Medicine, Brown University School of Medicine and the Miriam Hospital, 1992.

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Chapple, Christopher R., and Altaf Mangera. Urgency incontinence and overactive bladder. Edited by Christopher R. Chapple. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199659579.003.0040.

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Overactive bladder (OAB) is very prevalent and may be very bothersome. In this chapter, we describe the various definitions associated with this condition, its assessment and management. The definitions for lower urinary tract symptoms have been standardized by the International Continence Society. OAB is a symptomatic diagnosis after all other pathology has been excluded. Important assessments include a frequency volume chart and in some cases urodynamic studies. Here we describe the important parameters which should be sought from a frequency volume chart. In addition, the relationship to the urodynamic diagnosis provided by a cystometry study is explained. Thereafter we discuss the therapeutic options for OAB which include conservative measures, antimuscarinics, beta-3 agonists, intravesical botulinum toxin, neuromodulation, and surgery. The various management options including lifestyle changes, alpha antagonists, 5-alpha reductase inhibitors, antimuscarinics, desmopressin and surgery are also described.

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Carpenter, Douglas W. Childhood Trauma and the Non-Alpha Male - Gender Role Conflict, Toxic Shame, and Complex Trauma: Finding Hope, Clarity, Healing, and Change. Atlantic Publishing Group Inc., 2018.

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Fiers, Walter, and Wim A. Buurman. Tumor Necrosis Factor: Molecular and Cellular Biology and Clinical Relevance. S Karger Pub, 1993.

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Book chapters on the topic "Alpha toxin"

1

Bhakdi, Sucharit, Iwan Walev, Matthias Husmann, and Angela Valeva. "Staphylococcal alpha-toxin." In Microbial Protein Toxins, 91–110. Berlin, Heidelberg: Springer Berlin Heidelberg, 2004. http://dx.doi.org/10.1007/b100513.

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Titball, Richard W., Helen Yeoman, and Sophie E. C. Hunter. "Gene Cloning and Organization of the Alpha-Toxin of Clostridium perfringens." In Brock/Springer Series in Contemporary Bioscience, 211–26. New York, NY: Springer New York, 1993. http://dx.doi.org/10.1007/978-1-4615-7087-5_14.

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Nagahama, Masahiro, Sadayuki Ochi, Keiko Kobayashi, and Jun Sakurai. "The Relationship between Histidine Redidues and Various Biological Activities of Clostridium perfringens Alpha Toxin." In Advances in Experimental Medicine and Biology, 251–55. Boston, MA: Springer US, 1996. http://dx.doi.org/10.1007/978-1-4613-0361-9_19.

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Fernandez-Miyakawa, Mariano E., and Leandro M. Redondo. "Role of Clostridium perfringens Alpha, Beta, Epsilon and Iota toxins in Enterotoxemia of monogastrics and Ruminants." In Microbial Toxins, 1–26. Dordrecht: Springer Netherlands, 2016. http://dx.doi.org/10.1007/978-94-007-6725-6_16-1.

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Alvin, Joseph W., and D. Borden Lacy. "Role of Clostridium Perfringens Alpha, Beta, Epsilon and Lota Toxins in Enterotoxemia of Monogastrics and Ruminants." In Microbial Toxins, 1–18. Dordrecht: Springer Netherlands, 2016. http://dx.doi.org/10.1007/978-94-007-6725-6_26-1.

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Fernandez-Miyakawa, Mariano E., and Leandro M. Redondo. "Role of Clostridium perfringens Alpha, Beta, Epsilon, and Iota Toxins in Enterotoxemia of Monogastrics and Ruminants." In Toxinology, 93–118. Dordrecht: Springer Netherlands, 2018. http://dx.doi.org/10.1007/978-94-007-6449-1_16.

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Wilt, Susan G., Jia Min Zhou, Steve Wesselingh, Conrad V. Kufta, and Monique Dubois-Dalcq. "Tumor Necrosis Factor Alpha Derived from Human Microglia Enhances HIV-1 Replication and is Toxic for Rat Oligodendrocytes in Vitro." In Technical Advances in AIDS Research in the Human Nervous System, 151–62. Boston, MA: Springer US, 1995. http://dx.doi.org/10.1007/978-1-4615-1949-2_12.

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Prévost, Gilles, Mira Y. Tawk, Gaëlle Zimmermann-Meisse, and Emmanuel Jover. "The staphylococcal alpha-toxin and leukotoxins." In The Comprehensive Sourcebook of Bacterial Protein Toxins, 739–72. Elsevier, 2015. http://dx.doi.org/10.1016/b978-0-12-800188-2.00025-2.

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Harshman, Sidney, Nancy Sugg, and Paul Cassidy. "[1] Preparation and purification of staphylococcal alpha toxin." In Microbial Toxins: Tools in Enzymology, 3–7. Elsevier, 1988. http://dx.doi.org/10.1016/s0076-6879(88)65004-x.

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Jolivet-Reynaud, Colette, Hervé Moreau, and Joseph E. Alouf. "[14] Purification of alpha toxin from clostridium perfringens: Phospholipase C." In Microbial Toxins: Tools in Enzymology, 91–94. Elsevier, 1988. http://dx.doi.org/10.1016/s0076-6879(88)65017-8.

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Conference papers on the topic "Alpha toxin"

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Oshima, K., S. A. McMurtry, K. I. Michael, J. A. Hippensteel, G. Su, F. Zhang, A. R. Horswill, J. Liu, R. J. Linhardt, and E. P. Schmidt. "Circulating Heparan Sulfate Binds the Staphylococcus Aureus Toxin Alpha-Hemolysin (Hla), Attenuating Hla-Induced Pulmonary Endothelial Injury." In American Thoracic Society 2019 International Conference, May 17-22, 2019 - Dallas, TX. American Thoracic Society, 2019. http://dx.doi.org/10.1164/ajrccm-conference.2019.199.1_meetingabstracts.a1977.

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Nawroth, Peter P., Jerry Brett, Susan Steinberg, Charles T. Esmon, and David M. Stern. "ENDOTHELIUM AND PROTEIN S: SYNTHESIS, RELEASE AND REGULATION OF ANTICOAGULANT ACTIVITY." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1642962.

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The protein C-protein S pathway is closely linked to the vessel wall. In terms of protein C, endothelium has been shown to provide the receptor thrombomodulin, which promotes thrombin-mediated formation of activated protein C. Optimal anticoagulant function of activated protein C requires protein S and a cellular surface. Recent studies have indicated that endothelium can facilitate assembly of the activated protein C-protein S complex and that bovine endothelium expresses specific binding site(s) for protein S which promote its anticoagulant function. Expression of protein S binding sites is subject to down-regulation by Tumor Necrosis Factor (TNF) . Exposure of cultured bovine endothelium to TNF results in decreased 125I-protein s binding and attenuated rates of Factor Va inactivation after 2 hrs followed by negligible 125I-protein S binding and Factor Va inactivation by 10 hrs. These changes persist for over 48 hrs, in contrast to the more transient rise in endothelial cell tissue factor induced by TNF which returns to baseline by 24 hrs.In addition to providing binding sites for protein S, endothelium constitutively synthesizes and releases this vitamin K-dependent anticoagulant cofactor. Release of protein S is blocked by addition of warfarin, indicating that y-carboxylation facilitates the release of intracellular protein S. Morphologic studies, at the level of electron microscope, have shown protein S antigen to be present in cisternae of rough endoplasmic reticulum, the trans face of the golgi and a population of intracellular vesicles which appear to be distributed at the cellular periphery. By immunofluorescence, the distribution of protein S is distinct from that of von Willebrand Factor. The intracellular vesicles containing protein S constitute a storage pool potentially available for rapid release. Treatment of endothelium with norepinephrine results in release of protein S over the next 20 min. Release is half-maximal at a norepinephrine concentration of about 0.1 uM and is not observed with the biologically inactive entantiomer (+) norepinephrine. Norepinephrine-induced release of intracellular protein S can be blocked by prazosine (10-7 7 M), but not by propranolol (10-6 M) or yohimbine (10-5 M). These data are consistent with release of protein S being a receptor-mediated process dependent on an endothelial cell alpha 1 adrenergic receptor. Blockade of norepinephrine-induced release of protein S by pertussis toxin treatment of endothelium further defines the intracellular pathway of protein S and implicates regulatory G proteins in the stimulus-response coupling. Electron microscopic studies have shown that following exposure of endothelium to norepinephrine the intracellular vesicles containing protein S undergo exocytosis at the plasma membrane. These data define a new relationship between the autonomic nervous system and the coagulation mechanism.Protein S is clearly an endothelial cell-associated anticoagulant protein. A specific binding site on the endothelial cell surface can regulate its anticoagulant function on the vessel wall. Endothelial cell synthesis and release of protein S defines a new level of participation of endothelium in the protein C-protein S pathway.

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Cournoyer, Michael E., David L. Wannigman, and Robert L. Dodge. "Pollution Prevention Benefits of Dissolvable Protective Clothing." In ASME 2011 14th International Conference on Environmental Remediation and Radioactive Waste Management. ASMEDC, 2011. http://dx.doi.org/10.1115/icem2011-59003.

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Programmatic operations at the Los Alamos National Laboratory Plutonium Facility (TA-55) involve working with various amounts of plutonium and other highly toxic, alpha-emitting materials. The spread of radiological contamination on surfaces, airborne contamination, and excursions of contaminants into the operator’s breathing zone are controlled through the radiological protection program. A key element of this program is the proper selection of protective clothing. Re-useable, launderable protective clothing has been the standard for several decades. Over the years, radioactive waste disposal costs have increased and disposal options have become more limited. This has prompted the development of single-use, dissolvable protective clothing. Single-use, dissolvable protective clothing is under evaluation as a replacement for launderable woven textile garments at TA-55. We examined re-useable, launderable and single-use, dissolvable protective clothing, addressed management issues (residual contamination, cost, environmental footprint, quality assurance), and waste minimization benefits. Replacement of launderable garments with single-use, dissolvable protective clothing improves the safety configuration of TA-55 by reducing LLW waste generation.

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Makhoul-Mansour, Michelle M., and Eric C. Freeman. "Photo-Triggered Soft Materials With Differentiated Diffusive Pathways." In ASME 2019 Conference on Smart Materials, Adaptive Structures and Intelligent Systems. American Society of Mechanical Engineers, 2019. http://dx.doi.org/10.1115/smasis2019-5525.

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Abstract Controlled diffusive transport between regions within a compartmentalized structure is an essential feature of cellular-inspired materials. Using the droplet interface bilayer (DIB) technique, biomolecular soft materials can be constructed in an oil medium by connecting multiple lipid-coated microdroplets together through interfacial bilayers. While traditionally achieved through the incorporation of pore forming toxins (PFTs), signal propagation within DIB assemblies can be remotely controlled through the integration of photopolymerizable phospholipids (23:2 DiynePC) into the aqueous phase. Since such strategy allows for the formation of UV-C triggered pathways only between droplets both containing DiynePC, polymerizable phospholipids have shown an advantage of reducing undesired diffusion and forming conductive pathways. The partial polymerization of lipid bilayers formed through the DIB platform is still to this date underexplored in the literature. In a previous work, we have shown that the incorporation of 23:2 DiynePC into lipid bilayers allows for the creation of patterned conductive pathways in a 2D DIB structure. The properties of photosensitive bilayers were also investigated but not their channel activity. The functionalization of bilayers-based photosensitive structures through transmembrane channels remains an under-investigated mean of achieving further differentiated conductive channels. This work explores the reconstitution of several transmembrane channels such as alpha-hemolysin (αHL) and alamethicin (ALM) into partially polymerized lipid bilayers. We believe that the ability to incorporate transmembrane channels into photosensitive DIB soft structures allows for further differentiation of signal propagation pathways by including both edge-defect induced pores as well as more traditional and bio-derived transporters.

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Cournoyer, Michael E., Archie E. Nixon, Keith W. Fife, Arnold M. Sandoval, Vincent E. Garcia, and Robert L. Dodge. "Transuranic (TRU) Waste Volume Reduction Operation at a Plutonium Facility." In ASME 2010 13th International Conference on Environmental Remediation and Radioactive Waste Management. ASMEDC, 2010. http://dx.doi.org/10.1115/icem2010-40132.

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Programmatic operations at the Los Alamos National Laboratory Plutonium Facility (TA-55) involve working with various amounts of plutonium and other highly toxic, alpha-emitting materials. The spread of radiological contamination on surfaces, airborne contamination, and excursions of contaminants into the operator’s breathing zone are prevented through use of a variety of gloveboxes (the glovebox, coupled with an adequate negative pressure gradient, provides primary confinement). Size-reduction operations on glovebox equipment are a common activity when a process has been discontinued and the room is being modified to support a new customer. The Actinide Processing Group at TA-55 uses one-meter or longer glass columns to process plutonium. Disposal of used columns is a challenge, since they must be size-reduced to get them out of the glovebox. The task is a high-risk operation because the glass shards that are generated can puncture the bag-out bags, leather protectors, glovebox gloves, and the worker’s skin when completing the task. One of the Lessons Learned from these operations is that Laboratory management should critically evaluate each hazard and provide more effective measures to prevent personnel injury. A bag made of puncture-resistant material was one of these enhanced controls. We have investigated the effectiveness of these bags and have found that they safely and effectively permit glass objects to be reduced to small pieces with a plastic or rubber mallet; the waste can then be easily poured into a container for removal from the glovebox as non-compactable transuranic (TRU) waste. This size-reduction operation reduces solid TRU waste volume generation by almost 2-1/2 times. Replacing one-time-use bag-out bags with multiple-use glass crushing bags also contributes to reducing generated waste. In addition, significant costs from contamination, cleanup, and preparation of incident documentation are avoided. This effort contributes to the Los Alamos National Laboratory Continuous Improvement Program by improving the efficiency, cost-effectiveness, and formality of glovebox operations. In this report, the technical issues, associated with implementing this process improvement are addressed, the results discussed, effectiveness of Lessons Learned evaluated, and waste savings presented.

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Reports on the topic "Alpha toxin"

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Shor, J. T., S. P. N. Singh, and L. V. Jr Gibson. Progress report and technology status development of an EG and G Berthold LB-150 alpha/beta particulate monitor for use on the East Tennessee Technology Park Toxic Substances Control Act Incinerator. Office of Scientific and Technical Information (OSTI), June 1998. http://dx.doi.org/10.2172/638188.

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