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Relevant bibliographies by topics / Gas gangrene

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Academic literature on the topic 'Gas gangrene'

Author: Grafiati

Published: 4 June 2021

Last updated: 5 March 2023

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Journal articles on the topic "Gas gangrene"

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Jiang, Dongneng, Liqun Zhang, Fei Liu, Chang Liu, Linlin Liu, and Xiaoyun Pu. "An electrochemiluminescence sensor with dual signal amplification of Ru(bpy)32+based on PtNPs and glucose dehydrogenase for diagnosis of gas gangrene." RSC Advances 6, no. 24 (2016): 19676–85. http://dx.doi.org/10.1039/c5ra27241f.

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Gas gangrene is a bacterial infection that produces gas in tissues in gangrene.C. perfringenswith alpha-toxin plays a key role in gas gangrene. Detection ofC. perfringensis highly important in clinical diagnosis of gas gangrene.

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Stephens, Lt Mark B. "Gas gangrene." Postgraduate Medicine 99, no. 4 (April 1996): 217–24. http://dx.doi.org/10.1080/00325481.1996.11946109.

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Schexnayder, Stephen M., and Sarah G. Klein. "Gas Gangrene." New England Journal of Medicine 350, no. 25 (June 17, 2004): 2603. http://dx.doi.org/10.1056/nejmicm980151.

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Pitt, M., N. J. Purser, Gilles Bouachour, JeanPaul Gouello, Patrick Harry, and Philippe Alquier. "Gas gangrene." Lancet 347, no. 9008 (April 1996): 1116–17. http://dx.doi.org/10.1016/s0140-6736(96)90315-3.

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Coleman, D. J., and A. G. Batchelor. "Gas gangrene." BMJ 296, no. 6636 (June 4, 1988): 1600–1601. http://dx.doi.org/10.1136/bmj.296.6636.1600-a.

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Golledge, C., A. Keil, and T. McKenzie. "Gas gangrene." BMJ 296, no. 6636 (June 4, 1988): 1601. http://dx.doi.org/10.1136/bmj.296.6636.1601.

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Bignardi, G. E. "Gas gangrene." BMJ 296, no. 6637 (June 11, 1988): 1671. http://dx.doi.org/10.1136/bmj.296.6637.1671.

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Maddocks, J. L. "Gas gangrene." BMJ 297, no. 6642 (July 16, 1988): 204. http://dx.doi.org/10.1136/bmj.297.6642.204-c.

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Lehner, P. J., and H. Powell. "Gas gangrene." BMJ 303, no. 6796 (July 27, 1991): 240–42. http://dx.doi.org/10.1136/bmj.303.6796.240.

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Mercer, N., and D. M. Davies. "Gas gangrene." BMJ 303, no. 6806 (October 5, 1991): 854–55. http://dx.doi.org/10.1136/bmj.303.6806.854-b.

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Dissertations / Theses on the topic "Gas gangrene"

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Jepson, Marie Alice. "The role of the C-Domain of clostridium perfringens Î±-toxin." Thesis, Birkbeck (University of London), 2001. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.247080.

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Therit, Blair H. "Investigation of the role of the toxins perfringolysin O (PFO) and sialidase in Clostridium perfringens gas gangrene infections." Thesis, Virginia Tech, 2006. http://hdl.handle.net/10919/35136.

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Clostridium perfringens is the causative agent of gas gangrene. A lethal infection in mice requires a large inoculum suggesting that the immune system is involved in inhibiting disease. Human monocytic cells and neutrophils killed C. perfringens in vitro when complement was present. Macrophages and neutrophils co-localized with C. perfringens in vivo when bacterial numbers were low. Depletion of neutrophils and monocytes in mice revealed that monocytic cells play a role in inhibiting C. perfringens gas gangrene in mice infected with an intermediate dose. C. perfringens can persist in the tissues and this could be mediated by persistence within macrophages. To examine if the toxin perfringolysin O (PFO) could mediate this, less active variants of PFO were used to examine what occurs between phagosomal escape and cell lysis. The mutant forms of PFO did mediate phagosomal escape in macrophages and were found within macrophages at higher numbers than wild-type C. perfringens. Our data were preliminary but may indicate that less active PFO mediates intracellular persistence. To investigate the role of sialidase in C. perfringens gas gangrene we made nanI-, nanJ-, and nanI-/nanJ- mutants. We observed that NanI is responsible for the majority of sialidase activity of C. perfringens strain 13, that NanJ is an extracellular sialidase, and that these genes are transcriptionally regulated by sialic acid. Murine infection trials revealed that these sialidases may be protective for mice during infection. In conclusion, murine monocytes inhibit disease onset and C. perfringens sialidase enhances mouse survival. However, the toxin PFO if less active promotes the survival of C. perfringens with macrophages.
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Gatsos, Xenia, and xgatsos@optusnet com au. "The development of live vectored vaccines targeting the alpha-toxin of Clostridium perfringens for the prevention of necrotic enteritis in poultry." RMIT University. Applied Sciences, 2007. http://adt.lib.rmit.edu.au/adt/public/adt-VIT20080212.142403.

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The Ñ-toxin of Clostridium perfringens is a toxin involved in numerous diseases of humans and agriculturally important animals. One of these diseases is necrotic enteritis (NE), a sporadic enteric disease which affects avian species world-wide. This study involved the inactivation of alpha-toxin (Ñ-toxin) for use as a potential vaccine candidate to combat NE in chickens, and other diseases caused by C. perfringens type A. During the course of this research a number of Ñ-toxin recombinant proteins were developed through molecular inactivation of the Ñ-toxin gene, plc. Proteins plc316 and plc204 were developed by the deletion of the first three and seven Ñ-helices of the N-terminal domain respectively. These deletions resulted in proteins which were unstable in solution, constantly aggregated into insoluble masses and elicited lower overall antibody responses when administered to mice. A third protein, plcInv3 was developed from the deletion of part of the catalytic domain of the Ñ-toxin. PlcInv3 was highly soluble and upon immunisation of mice elicited a significant antibody response which was also capable of protecting mice against a live challenge of C. perfringens. The fourth and final protein developed was plc104. The smallest of the recombinant Ñ-toxin proteins, it consisted entirely of the C-terminal domain of Ñ-toxin. Its small size did not affect its ability to induce a strong antibody response when administered to mice, the antibodies of which were also protective during a challenge with C. perfringens. STM1, an attenuated strain of S. Typhimurium was used in the development of a vectored vaccine for the expression and oral delivery of plcInv3 and plc104 within the mouse host. The proteins were expressed within STM1 from expression plasmids containing the in vivo inducible promoters PhtrA and PpagC. A measurable humoral immune response against Ñ-toxin was absent following three oral vaccinations with the vectored vaccines, although, cytokine profiling of splenocytes from vaccinated mice revealed an increase in the number of interleukin-4 (IL-4)secreting cells and the lack of interferon-gamma (IFN-×) secreting cells. This indicated the stimulation of a T-helper type 2 (TH2) immune response which also lead to partial protection against a live C. perfringens challenge. This study demonstrates the feasibility of using STM1 as a carrier for the in vivo expression of the C. perfringens Ñ-toxin recombinant proteins plcInv3 and plc104. It is the first study to express C. perfringens antigens within an attenuated strain of S. Typhimurium, STM1.The partial protection of mice immunised with these vaccines indicates there is potential for this vectored vaccine system to be used in the protection of diseases caused by the Ñ-toxin of C. perfringens.

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Books on the topic "Gas gangrene"

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Parker, Philip M., and James N. Parker. Gas gangrene: A medical dictionary, bibliography, and annotated research guide to Internet references. San Diego, CA: ICON Health Publications, 2004.

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Publications, ICON Health. Gas Gangrene - A Medical Dictionary, Bibliography, and Annotated Research Guide to Internet References. ICON Health Publications, 2004.

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Harrison, Mark. Clostridial infection. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780198765875.003.0015.

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This chapter describes the microbiology of clostridial infection as it applies to Emergency Medicine, and in particular the Primary FRCEM examination. The chapter outlines the key details of the source, clinical features, and principles of treatment and prevention of clostridial colitis, clostridial gas gangrene, and tetanus. This chapter is laid out exactly following the RCEM syllabus, to allow easy reference and consolidation of learning.

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Wilson-MacDonald, James, and Andrew James. Complications of fractures. Oxford University Press, 2011. http://dx.doi.org/10.1093/med/9780199550647.003.012002.

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♦ Fat embolism syndrome is defined as the presence of globules of fat in the lungs and in other tissues and occurs occasionally in long bone fractures♦ Reflex sympathetic dystrophy is characterized by intense prolonged pain, vasomotor disturbance, delayed functional recovery, and trophic changes♦ Avascular necrosis typically affects intra-articular bone after fracture and can occur in up to 70% of displaced talar neck fractures♦ Immobility associated with recovery from fracture is associated with deep vein thrombosis, which carries a risk of pulmonary embolism, and should be treated with anti-coagulants♦ Gas gangrene is a rapidly-spreading infection of devitalized tissue, removal of the affected area and treatment with penicillin is required♦ Compartment syndrome within a closed compartment can result in tissue ischaemia and necrosis followed by fibrosis and muscle contracture

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Book chapters on the topic "Gas gangrene"

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Order, Stanley E., and Sarah S. Donaldson. "Gas Gangrene." In Radiation Therapy of Benign Diseases, 111. Berlin, Heidelberg: Springer Berlin Heidelberg, 2003. http://dx.doi.org/10.1007/978-3-642-58719-1_46.

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Bensard, Denis D., Kathryn M. Beauchamp, Ryan T. Hurt, Stephen A. McClave, Angela M. Mills, Esther H. Chen, J. P. J. Wester, et al. "Gas Gangrene." In Encyclopedia of Intensive Care Medicine, 964. Berlin, Heidelberg: Springer Berlin Heidelberg, 2012. http://dx.doi.org/10.1007/978-3-642-00418-6_1632.

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Gooch, Jan W. "Gas Gangrene." In Encyclopedic Dictionary of Polymers, 895. New York, NY: Springer New York, 2011. http://dx.doi.org/10.1007/978-1-4419-6247-8_13808.

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Gupta, Parmanand, and Hitesh Shah. "Gas Gangrene." In Pediatric Musculoskeletal Infections, 761–71. Cham: Springer International Publishing, 2022. http://dx.doi.org/10.1007/978-3-030-95794-0_37.

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George, W. Lance, and Sydney M. Finegold. "Clostridial Myconecrosis (Gas Gangrene)." In Laboratory Diagnosis of Infectious Diseases, 202–4. New York, NY: Springer New York, 1988. http://dx.doi.org/10.1007/978-1-4612-3898-0_20.

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Silva, Rodrigo O. S., Francisco A. Uzal, Carlos A. Oliveira, and Francisco C. F. Lobato. "Gas Gangrene (Malignant Edema)." In Clostridial Diseases of Animals, 243–54. Hoboken, NJ: John Wiley & Sons, Inc, 2016. http://dx.doi.org/10.1002/9781118728291.ch20.

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Ratliff, A. H. C., J. H. Dixon, P. A. Magnussen, and S. K. Young. "Tetanus and Gas Gangrene." In Selected References in Orthopaedic Trauma, 26. London: Springer London, 1989. http://dx.doi.org/10.1007/978-1-4471-1695-0_11.

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Giri, Biplab, and Labanyamoy Kole. "Combating the Perilous Consequence of Clostridial Gas Gangrene: An Overview." In Toxinology, 1–21. Dordrecht: Springer Netherlands, 2014. http://dx.doi.org/10.1007/978-94-007-6645-7_36-1.

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Giri, Biplab, and Labanyamoy Kole. "Combating the Insidious Enemy: Epidemiology, Pathophysiology, and Treatment of Clostridial Gas Gangrene." In Biological Toxins and Bioterrorism, 425–48. Dordrecht: Springer Netherlands, 2014. http://dx.doi.org/10.1007/978-94-007-5869-8_36.

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Galoyan, Armen A. "Treatment of Clostridium Perfringens-induced Gas Gangrene by New Cytokines of Brain." In Advances in Neurobiology, 103–19. New York, NY: Springer New York, 2012. http://dx.doi.org/10.1007/978-1-4614-3667-6_7.

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Reports on the topic "Gas gangrene"

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Muhvich, K. H., L. H. Anderson, and W. J. Mehm. Combined Effects of Hyperbaric Oxygen and Antimicrobials in a Model of Gas Gangrene. Fort Belvoir, VA: Defense Technical Information Center, June 1992. http://dx.doi.org/10.21236/ada253610.

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