vickram ramkumar (20 Ergebnisse)

PAP. Zustand: New. New Book. Shipped from UK. Established seller since 2000.

PAP. Zustand: New. New Book. Shipped from UK. Established seller since 2000.

Zustand: New. In.

Zustand: New. In.

Zustand: NEW.

Paperback. Zustand: Brand New. reprint edition. 9.25x6.10 inches. In Stock.

Zustand: 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.

Hardcover. Zustand: Brand New. 244 pages. 9.25x6.10x0.67 inches. In Stock.

Taschenbuch. Zustand: 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.

Buch. Zustand: 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.

Taschenbuch. Zustand: 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.

Zustand: New. This is a Brand-new US Edition. This Item may be shipped from US or any other country as we have multiple locations worldwide.

HRD. Zustand: New. New Book. Shipped from UK. Established seller since 2000.

Zustand: Used. pp. 450.

HRD. Zustand: New. New Book. Shipped from UK. Established seller since 2000.

Zustand: Used. pp. 450.

Hardcover. Zustand: Brand New. 1st edition. 373 pages. 9.75x7.00x1.00 inches. In Stock.

Gebunden. Zustand: New. KlappentextrnrnThe role of adenosine and adenosine receptors in normal cell physiology and in diseases has been an area of active research over the last several decades. The field has advanced from the use of limited tools to examine receptor si.

Zustand: New. Editor(s): Ramkumar, Vickram; Paes De Carvalho, Roberto. Num Pages: 450 pages. BIC Classification: MMG; MMZ. Category: (P) Professional & Vocational. Dimension: 260 x 180. Weight in Grams: 854. . 2015. 1st Edition. Hardcover. . . . . Books ship from the US and Ireland.

Buch. Zustand: Neu. Neuware - The role of adenosine and adenosine receptors in normal cell physiology and in diseases has been an area of active research over the last several decades. The field has advanced from the use of limited tools to examine receptor signaling and function to the use of various molecular and receptor knockout techniques to examine the details of the expression and functions and regulation of these receptors. This book highlights important milestones in adenosine receptor research and reviews recent findings from experts in different research areas. Several research areas, ranging from cardiovascular, cancer, and central nervous system research are discussed. Several of the chapters describe how understanding the basic cellular mechanisms regulated by adenosine could lead to the development of important therapeutics. The editors, Vickram Ramkumar and Roberto Paes-de-Carvalho, have published extensively on adenosine receptors for more than two decades and are still active in this field of research. It is our hope that this book provides an excellent synopsis of the current status of adenosine receptor research which would be valuable for researchers in the field and as a reference source for clinicians and others interested in this area.