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  1. Book ; Online ; E-Book: Inflammatory mechanisms in mediating hearing loss

    Ramkumar, Vickram / Rybak, Leonard P.

    2018  

    Author's details Vickram Ramkumar, Leonard P. Rybak editors
    Keywords Medicine ; Neurosciences ; Otorhinolaryngology
    Subject code 612.8
    Language English
    Size 1 Online-Ressource (x, 231 Seiten), Illustrationen
    Publisher Springer
    Publishing place Cham
    Publishing country Switzerland
    Document type Book ; Online ; E-Book
    Remark Zugriff für angemeldete ZB MED-Nutzerinnen und -Nutzer
    HBZ-ID HT019789105
    ISBN 978-3-319-92507-3 ; 9783319925066 ; 3-319-92507-5 ; 3319925067
    DOI 10.1007/978-3-319-92507-3
    Database ZB MED Catalogue: Medicine, Health, Nutrition, Environment, Agriculture

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  2. Book: Free radicals in ENT pathology

    Miller, Josef / Le Prell, Colleen G. / Rybak, Leonard P.

    (Oxidative stress in applied basic research and clinical practice)

    2015  

    Author's details Josef Miller ; Colleen G. Le Prell ; Leonard Rybak
    Series title Oxidative stress in applied basic research and clinical practice
    Language English
    Size XIV, 507 S. : Ill., graph. Darst.
    Publisher Humana Press
    Publishing place Cham u.a.
    Publishing country Switzerland
    Document type Book
    HBZ-ID HT018650038
    ISBN 978-3-319-13472-7 ; 9783319134734 ; 3-319-13472-8 ; 3319134736
    Database Catalogue ZB MED Medicine, Health

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    In stock of ZB MED Cologne/Königswinter

    Shelf markLoan statusLocation
    2015 A 1869 available for loan (reading room) Lesesaal EG

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  3. Article: Ototoxicity of Non-aminoglycoside Antibiotics.

    Rybak, Leonard P / Ramkumar, Vickram / Mukherjea, Debashree

    Frontiers in neurology

    2021  Volume 12, Page(s) 652674

    Abstract: It is well-known that aminoglycoside antibiotics can cause significant hearing loss and vestibular deficits that have been described in animal studies and in clinical reports. The purpose of this review is to summarize relevant preclinical and clinical ... ...

    Abstract It is well-known that aminoglycoside antibiotics can cause significant hearing loss and vestibular deficits that have been described in animal studies and in clinical reports. The purpose of this review is to summarize relevant preclinical and clinical publications that discuss the ototoxicity of non-aminoglycoside antibiotics. The major classes of antibiotics other than aminoglycosides that have been associated with hearing loss in animal studies and in patients are discussed in this report. These antibiotics include: capreomycin, a polypeptide antibiotic that has been used to treat patients with drug-resistant tuberculosis, particularly in developing nations; the macrolides, including erythromycin, azithromycin and clarithromycin; and vancomycin. These antibiotics have been associated with ototoxicity, particularly in neonates. It is critical to be aware of the ototoxic potential of these antibiotics since so much attention has been given to the ototoxicity of aminoglycoside antibiotics in the literature.
    Language English
    Publishing date 2021-03-09
    Publishing country Switzerland
    Document type Journal Article ; Review
    ZDB-ID 2564214-5
    ISSN 1664-2295
    ISSN 1664-2295
    DOI 10.3389/fneur.2021.652674
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Article ; Online: Effects of natural products on cisplatin ototoxicity and chemotherapeutic efficacy.

    Rybak, Leonard P / Alberts, Ian / Patel, Shree / Al Aameri, Raheem F H / Ramkumar, Vickram

    Expert opinion on drug metabolism & toxicology

    2023  Volume 19, Issue 9, Page(s) 635–652

    Abstract: Introduction: Cisplatin is a very effective chemotherapeutic agent against a variety of solid tumors. Unfortunately, cisplatin causes permanent sensorineural hearing loss in at least two-thirds of patients treated. There are no FDA approved drugs to ... ...

    Abstract Introduction: Cisplatin is a very effective chemotherapeutic agent against a variety of solid tumors. Unfortunately, cisplatin causes permanent sensorineural hearing loss in at least two-thirds of patients treated. There are no FDA approved drugs to prevent this serious side effect.
    Areas covered: This paper reviews various natural products that ameliorate cisplatin ototoxicity. These compounds are strong antioxidants and anti-inflammatory agents. This review includes mostly preclinical studies but also discusses a few small clinical trials with natural products to minimize hearing loss from cisplatin chemotherapy in patients. The interactions of natural products with cisplatin in tumor-bearing animal models are highlighted. A number of natural products did not interfere with cisplatin anti-tumor efficacy and some agents actually potentiated cisplatin anti-tumor activity.
    Expert opinion: There are a number of natural products or their derivatives that show excellent protection against cisplatin ototoxicity in preclinical studies. There is a need to insure uniform standards for purity of drugs derived from natural sources and to ensure adequate pharmacokinetics and safety of these products. Natural products that protect against cisplatin ototoxicity and augment cisplatin's anti-tumor effects in multiple studies of tumor-bearing animals are most promising for advancement to clinical trials. The most promising natural products include honokiol, sulforaphane, and thymoquinone.
    Language English
    Publishing date 2023-10-12
    Publishing country England
    Document type Journal Article ; Review
    ZDB-ID 2214462-6
    ISSN 1744-7607 ; 1742-5255
    ISSN (online) 1744-7607
    ISSN 1742-5255
    DOI 10.1080/17425255.2023.2260737
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 6264: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
    bis Jg. 2021: Bestellungen von Artikeln über das Online-Bestellformular
    ab Jg. 2022: Lesesaal (EG)

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  5. Book: Ototoxicity

    Rybak, Leonard P.

    (The otolaryngologic clinics of North America ; 26,5)

    1993  

    Author's details Leonard P. Rybak, guest ed
    Series title The otolaryngologic clinics of North America ; 26,5
    Otolaryngologic clinics of North America
    Collection Otolaryngologic clinics of North America
    Keywords Ear / drug effects ; Ear Diseases / chemically induced ; Drugs / adverse effects
    Language English
    Size VIII S., S. 705 - 918 : Ill., graph. Darst.
    Publisher Saunders
    Publishing place Philadelphia u.a.
    Publishing country United States
    Document type Book
    HBZ-ID HT005030749
    Database Catalogue ZB MED Medicine, Health

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    In stock of ZB MED Cologne/Königswinter

    Shelf markLoan statusLocation
    Zs B 183 -26,5- verfügbar in Königswinter Königswinter

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  6. Article: Oxidative Stress and Inflammation Caused by Cisplatin Ototoxicity.

    Ramkumar, Vickram / Mukherjea, Debashree / Dhukhwa, Asmita / Rybak, Leonard P

    Antioxidants (Basel, Switzerland)

    2021  Volume 10, Issue 12

    Abstract: Hearing loss is a significant health problem that can result from a variety of exogenous insults that generate oxidative stress and inflammation. This can produce cellular damage and impairment of hearing. Radiation damage, ageing, damage produced by ... ...

    Abstract Hearing loss is a significant health problem that can result from a variety of exogenous insults that generate oxidative stress and inflammation. This can produce cellular damage and impairment of hearing. Radiation damage, ageing, damage produced by cochlear implantation, acoustic trauma and ototoxic drug exposure can all generate reactive oxygen species in the inner ear with loss of sensory cells and hearing loss. Cisplatin ototoxicity is one of the major causes of hearing loss in children and adults. This review will address cisplatin ototoxicity. It includes discussion of the mechanisms associated with cisplatin-induced hearing loss including uptake pathways for cisplatin entry, oxidative stress due to overpowering antioxidant defense mechanisms, and the recently described toxic pathways that are activated by cisplatin, including necroptosis and ferroptosis. The cochlea contains G-protein coupled receptors that can be activated to provide protection. These include adenosine A1 receptors, cannabinoid 2 receptors (CB2) and the Sphingosine 1-Phosphate Receptor 2 (S1PR2). A variety of heat shock proteins (HSPs) can be up-regulated in the cochlea. The use of exosomes offers a novel method of delivery of HSPs to provide protection. A reversible MET channel blocker that can be administered orally may block cisplatin uptake into the cochlear cells. Several protective agents in preclinical studies have been shown to not interfere with cisplatin efficacy. Statins have shown efficacy in reducing cisplatin ototoxicity without compromising patient response to treatment. Additional clinical trials could provide exciting findings in the prevention of cisplatin ototoxicity.
    Language English
    Publishing date 2021-11-29
    Publishing country Switzerland
    Document type Journal Article ; Review
    ZDB-ID 2704216-9
    ISSN 2076-3921
    ISSN 2076-3921
    DOI 10.3390/antiox10121919
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  7. Book: Furosemide ototoxicity

    Rybak, Leonard P.

    clinical and experimental aspects

    (Laryngoscope : Supplement ; 38)

    1985  

    Series title Laryngoscope : Supplement ; 38
    The laryngoscope
    Laryngoscope ; Supplement
    Collection The laryngoscope
    Laryngoscope ; Supplement
    Keywords Ear / drug effects ; Furosemide / toxicity
    Size 14 S. : graph. Darst.
    Publisher Laryngoscope
    Publishing place St. Louis, Mo
    Publishing country United States
    Document type Book
    HBZ-ID HT002117152
    Database Catalogue ZB MED Medicine, Health

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    In stock of ZB MED Cologne/Königswinter

    Shelf markLoan statusLocation
    Ul II Zs 82 -Suppl.38- verfügbar in Königswinter Königswinter

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  8. Article: Mechanisms of Cisplatin-Induced Ototoxicity and Prevention.

    Rybak, Leonard P / Mukherjea, Debashree / Ramkumar, Vickram

    Seminars in hearing

    2019  Volume 40, Issue 2, Page(s) 197–204

    Abstract: Cisplatin is a highly effective antineoplastic agent used to treat solid tumors. Unfortunately, the administration of this drug leads to significant side effects, including ototoxicity, nephrotoxicity, and neurotoxicity. This review addresses the ... ...

    Abstract Cisplatin is a highly effective antineoplastic agent used to treat solid tumors. Unfortunately, the administration of this drug leads to significant side effects, including ototoxicity, nephrotoxicity, and neurotoxicity. This review addresses the mechanisms of cisplatin-induced ototoxicity and various strategies tested to prevent this distressing adverse effect. The molecular pathways underlying cisplatin ototoxicity are still being investigated. Cisplatin enters targeted cells in the cochlea through the action of several transporters. Once it enters the cochlea, cisplatin is retained for months to years. It can cause DNA damage, inhibit protein synthesis, and generate reactive oxygen species that can lead to inflammation and apoptosis of outer hair cells, resulting in permanent hearing loss. Strategies to prevent cisplatin ototoxicity have utilized antioxidants, transport inhibitors, G-protein receptor agonists, and anti-inflammatory agents. There are no FDA-approved drugs to prevent cisplatin ototoxicity. It is critical that potential protective agents do not interfere with the antitumor efficacy of cisplatin.
    Language English
    Publishing date 2019-04-26
    Publishing country United States
    Document type Journal Article ; Review
    ZDB-ID 604961-8
    ISSN 1098-8955 ; 0734-0451
    ISSN (online) 1098-8955
    ISSN 0734-0451
    DOI 10.1055/s-0039-1684048
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.B 2630: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
    bis Jg. 2021: Bestellungen von Artikeln über das Online-Bestellformular
    ab Jg. 2022: Lesesaal (EG)
    Zs.MO 115: Show issues

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  9. Article ; Online: Targeting CXCL1 chemokine signaling for treating cisplatin ototoxicity.

    Al Aameri, Raheem F H / Alanisi, Entkhab M A / Oluwatosin, Adu / Al Sallami, Dheyaa / Sheth, Sandeep / Alberts, Ian / Patel, Shree / Rybak, Leonard P / Ramkumar, Vickram

    Frontiers in immunology

    2023  Volume 14, Page(s) 1125948

    Abstract: Cisplatin is chemotherapy used for solid tumor treatment like lung, bladder, head and neck, ovarian and testicular cancers. However, cisplatin-induced ototoxicity limits the utility of this agent in cancer patients, especially when dose escalations are ... ...

    Abstract Cisplatin is chemotherapy used for solid tumor treatment like lung, bladder, head and neck, ovarian and testicular cancers. However, cisplatin-induced ototoxicity limits the utility of this agent in cancer patients, especially when dose escalations are needed. Ototoxicity is associated with cochlear cell death through DNA damage, the generation of reactive oxygen species (ROS) and the consequent activation of caspase, glutamate excitotoxicity, inflammation, apoptosis and/or necrosis. Previous studies have demonstrated a role of CXC chemokines in cisplatin ototoxicity. In this study, we investigated the role of CXCL1, a cytokine which increased in the serum and cochlea by 24 h following cisplatin administration. Adult male Wistar rats treated with cisplatin demonstrated significant hearing loss, assessed by auditory brainstem responses (ABRs), hair cell loss and loss of ribbon synapse. Immunohistochemical studies evaluated the levels of CXCL1 along with increased presence of CD68 and CD45-positive immune cells in cochlea. Increases in CXCL1 was time-dependent in the spiral ganglion neurons and organ of Corti and was associated with progressive increases in CD45, CD68 and IBA1-positive immune cells. Trans-tympanic administration of SB225002, a chemical inhibitor of CXCR2 (receptor target for CXCL1) reduced immune cell migration, protected against cisplatin-induced hearing loss and preserved hair cell integrity. We show that SB225002 reduced the expression of
    MeSH term(s) Rats ; Animals ; Male ; Cisplatin/adverse effects ; Chemokine CXCL1/genetics ; Ototoxicity/drug therapy ; Ototoxicity/etiology ; Rats, Wistar ; NADPH Oxidases/metabolism ; Hearing Loss/chemically induced ; Hearing Loss/metabolism
    Chemical Substances Cisplatin (Q20Q21Q62J) ; SB 225002 ; Chemokine CXCL1 ; NADPH Oxidases (EC 1.6.3.-) ; Cxcl1 protein, rat
    Language English
    Publishing date 2023-03-31
    Publishing country Switzerland
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, N.I.H., Extramural
    ZDB-ID 2606827-8
    ISSN 1664-3224 ; 1664-3224
    ISSN (online) 1664-3224
    ISSN 1664-3224
    DOI 10.3389/fimmu.2023.1125948
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  10. Article: Local Drug Delivery for Prevention of Hearing Loss.

    Rybak, Leonard P / Dhukhwa, Asmita / Mukherjea, Debashree / Ramkumar, Vickram

    Frontiers in cellular neuroscience

    2019  Volume 13, Page(s) 300

    Abstract: Systemic delivery of therapeutics for targeting the cochlea to prevent or treat hearing loss is challenging. Systemic drugs have to cross the blood-labyrinth barrier (BLB). BLB can significantly prevent effective penetration of drugs in appropriate ... ...

    Abstract Systemic delivery of therapeutics for targeting the cochlea to prevent or treat hearing loss is challenging. Systemic drugs have to cross the blood-labyrinth barrier (BLB). BLB can significantly prevent effective penetration of drugs in appropriate concentrations to protect against hearing loss caused by inflammation, ototoxic drugs, or acoustic trauma. This obstacle may be obviated by local administration of protective agents. This route can deliver higher concentration of drug compared to systemic application and preclude systemic side effects. Protective agents have been administered by intra-tympanic injection in numerous preclinical studies. Drugs such as steroids, etanercept, D and L-methionine, pifithrin-alpha, adenosine agonists, melatonin, kenpaullone (a cyclin-dependent kinase 2 (CDK2) inhibitor) have been reported to show efficacy against cisplatin ototoxicity in animal models. Several siRNAs have been shown to ameliorate cisplatin ototoxicity when administered by intra-tympanic injection. The application of corticosteroids and a number of other drugs with adjuvants appears to enhance efficacy. Administration of siRNAs to knock down AMPK kinase, liver kinase B1 (LKB1) or G9a in the cochlea have been found to ameliorate noise-induced hearing loss. The local administration of these compounds appears to be effective in protecting the cochlea against damage from cisplatin or noise trauma. Furthermore the intra-tympanic route yields maximum protection in the basal turn of the cochlea which is most vulnerable to cisplatin ototoxicity and noise trauma. There appears to be very little transfer of these agents to the systemic circulation. This would avoid potential side effects including interference with anti-tumor efficacy of cisplatin. Nanotechnology offers strategies to effectively deliver protective agents to the cochlea. This review summarizes the pharmacology of local drug delivery by intra-tympanic injection to prevent hearing loss caused by cisplatin and noise exposure in animals. Future refinements in local protective agents provide exciting prospects for amelioration of hearing loss resulting from cisplatin or noise exposure.
    Language English
    Publishing date 2019-07-09
    Publishing country Switzerland
    Document type Journal Article ; Review
    ZDB-ID 2452963-1
    ISSN 1662-5102
    ISSN 1662-5102
    DOI 10.3389/fncel.2019.00300
    Database MEDical Literature Analysis and Retrieval System OnLINE

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