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Aggiungi al carrelloCondizione: As New. Unread book in perfect condition.
Lingua: Inglese
Editore: Springer Nature Switzerland AG, CH, 2019
ISBN 10: 3030064476 ISBN 13: 9783030064471
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Aggiungi al carrelloPaperback. Condizione: New. Softcover Reprint of the Original 1st 2018 ed.
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Aggiungi al carrelloPaperback. Condizione: Brand New. reprint edition. 9.25x6.10 inches. In Stock.
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Aggiungi al carrelloCondizione: As New. Unread book in perfect condition.
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ISBN 10: 3030064476 ISBN 13: 9783030064471
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Aggiungi al carrelloCondizione: New. Details several different aspects of the cochlear inflammatory processDiscusses recent clinical trials focusing on the use of anti-inflammatory agents for the treatment of drug, noise-induced and auto-immune mediated hearing loss.
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Aggiungi al carrelloHardcover. Condizione: Brand New. 244 pages. 9.25x6.10x0.67 inches. In Stock.
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Aggiungi al carrelloTaschenbuch. Condizione: Neu. Inflammatory Mechanisms in Mediating Hearing Loss | Vickram Ramkumar (u. a.) | Taschenbuch | x | Englisch | 2019 | Springer | EAN 9783030064471 | Verantwortliche Person für die EU: Springer Verlag GmbH, Tiergartenstr. 17, 69121 Heidelberg, juergen[dot]hartmann[at]springer[dot]com | Anbieter: preigu.
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Aggiungi al carrelloCondizione: New. Brand New! Fast Delivery This is an International Edition and ship within 24-48 hours. Deliver by FedEx and Dhl, & Aramex, UPS, & USPS and we do accept APO and PO BOX Addresses. Order can be delivered worldwide within 6-10 days and we do have flat rate for up to 2LB. Extra shipping charges will be requested if the Book weight is more than 5 LB. This Item May be shipped from India, United states & United Kingdom. Depending on your location and availability.
Lingua: Inglese
Editore: Springer International Publishing, Springer International Publishing, 2018
ISBN 10: 3319925067 ISBN 13: 9783319925066
Da: AHA-BUCH GmbH, Einbeck, Germania
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Aggiungi al carrelloBuch. Condizione: Neu. Druck auf Anfrage Neuware - Printed after ordering - Common forms of preventable hearing loss are drug and noise-induced hearing loss which are believed to be produced by a similar mechanism. The generation of reactive oxygen species appears to be a common mechanism mediating hearing loss produced by these different sources. As such, a number of laboratories have focused their research towards identifying the sources of ROS production in the cochlea following administration of chemotherapeutic agents or noise exposure. This led to the identification of ROS generating enzymes, such as xanthine oxidases, nitric oxide synthase, and NADPH oxidases which are activated and/or induced during the development of hearing loss. A consequence of these findings was the implementation of antioxidants in preclinical studies for the treatment of hearing loss. These antioxidants have provided different levels of protection in animal and human studies, but none of these have been approved by the US Food and Drug Administration for the treatmentof hearing loss. More recently, it was shown that noise-induced hearing loss was associated with recruitment of inflammatory cells and mediators in the cochlea. This finding would suggest that noise could produce injury to the cochlea which stimulates local and/or circulating inflammatory cells. A similar finding was observed in the cochlea following administration of the anticancer drug, cisplatin. In addition, our laboratory and others have provided a plausible mechanism by which noise or chemotherapeutic agents could stimulate the inflammatory response. Surprisingly, this mechanism involves ROS activation of transcription factors linked to inflammatory processes in the cochlea. These studies have led to the use of anti-inflammatory agents for the treatment of hearing loss. Preliminary studies targeting inflammatory cytokines appear especially promising in preclinical studies. A primary goal of this project is to describe our current understanding of theoxidant hypothesis of noise and drug-induced hearing loss and show how this relates to cochlear inflammation. Several different aspects of the cochlear inflammatory process will be discussed in detail, ranging from the sources of inflammatory cells, chemokines, inflammatory cytokines, and cochlea resident immune cells. Molecular pathways leading to activation of the local inflammatory process will be highlighted and treatment options will be discussed. The relevance of certain clinically used anti-inflammatory interventions, such as trans-typmanic steroids will also be discussed. Furthermore, we will examine recent patents focusing on the use of anti-inflammatory agents for the treatment of drug and noise-induced hearing loss.
Lingua: Inglese
Editore: Springer International Publishing, Springer International Publishing, 2019
ISBN 10: 3030064476 ISBN 13: 9783030064471
Da: AHA-BUCH GmbH, Einbeck, Germania
EUR 106,99
Quantità: 1 disponibili
Aggiungi al carrelloTaschenbuch. Condizione: Neu. Druck auf Anfrage Neuware - Printed after ordering - Common forms of preventable hearing loss are drug and noise-induced hearing loss which are believed to be produced by a similar mechanism. The generation of reactive oxygen species appears to be a common mechanism mediating hearing loss produced by these different sources. As such, a number of laboratories have focused their research towards identifying the sources of ROS production in the cochlea following administration of chemotherapeutic agents or noise exposure. This led to the identification of ROS generating enzymes, such as xanthine oxidases, nitric oxide synthase, and NADPH oxidases which are activated and/or induced during the development of hearing loss. A consequence of these findings was the implementation of antioxidants in preclinical studies for the treatment of hearing loss. These antioxidants have provided different levels of protection in animal and human studies, but none of these have been approved by the US Food and Drug Administration for the treatmentof hearing loss. More recently, it was shown that noise-induced hearing loss was associated with recruitment of inflammatory cells and mediators in the cochlea. This finding would suggest that noise could produce injury to the cochlea which stimulates local and/or circulating inflammatory cells. A similar finding was observed in the cochlea following administration of the anticancer drug, cisplatin. In addition, our laboratory and others have provided a plausible mechanism by which noise or chemotherapeutic agents could stimulate the inflammatory response. Surprisingly, this mechanism involves ROS activation of transcription factors linked to inflammatory processes in the cochlea. These studies have led to the use of anti-inflammatory agents for the treatment of hearing loss. Preliminary studies targeting inflammatory cytokines appear especially promising in preclinical studies. A primary goal of this project is to describe our current understanding of theoxidant hypothesis of noise and drug-induced hearing loss and show how this relates to cochlear inflammation. Several different aspects of the cochlear inflammatory process will be discussed in detail, ranging from the sources of inflammatory cells, chemokines, inflammatory cytokines, and cochlea resident immune cells. Molecular pathways leading to activation of the local inflammatory process will be highlighted and treatment options will be discussed. The relevance of certain clinically used anti-inflammatory interventions, such as trans-typmanic steroids will also be discussed. Furthermore, we will examine recent patents focusing on the use of anti-inflammatory agents for the treatment of drug and noise-induced hearing loss.
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EUR 164,11
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Aggiungi al carrelloCondizione: New. In.
Condizione: New.
Lingua: Inglese
Editore: Springer International Publishing, 2016
ISBN 10: 3319377132 ISBN 13: 9783319377131
Da: moluna, Greven, Germania
EUR 136,16
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Aggiungi al carrelloKartoniert / Broschiert. Condizione: New.
Lingua: Inglese
Editore: Springer International Publishing, 2015
ISBN 10: 3319134728 ISBN 13: 9783319134727
Da: moluna, Greven, Germania
EUR 136,16
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Aggiungi al carrelloGebunden. Condizione: New.
Lingua: Inglese
Editore: Springer Nature Switzerland AG, CH, 2019
ISBN 10: 3030064476 ISBN 13: 9783030064471
Da: Rarewaves.com UK, London, Regno Unito
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Aggiungi al carrelloPaperback. Condizione: New. Softcover Reprint of the Original 1st 2018 ed.
Da: Buchpark, Trebbin, Germania
EUR 98,00
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Aggiungi al carrelloCondizione: Sehr gut. Zustand: Sehr gut | Seiten: 524 | Sprache: Englisch | Produktart: Bücher | This comprehensive volume examines the current state of free radical biology and its impact on otology, laryngology, and head and neck function. The chapters collectively highlight the interrelationship of basic and translational studies in each area, define the challenges to translation, and identify the existing basic issues that demand investigation as well as the opportunities for novel intervention to prevent and treat ENT pathology and impairment. In each chapter, or in some cases pairs of chapters, the author(s) have included or married issues of basic research with translational challenges and research, thus defining the pathway by which new basic insights may lead to interventions to prevent or treat impairment. The final chapter of this book reflects a meeting of all the contributors, culminating in a discussion and ¿white paper¿ that identifies the challenges to the field and defines the studies and collaborations that may lead to improved understanding of free radical biology in ENT and, subsequently, new interventions to medically treat ENT pathology.