Atjaunināt sīkdatņu piekrišanu

E-grāmata: Anticandidal Agents

(Associate Professor, Department of Biotechnology, National Institute of Technology Raipur, India)
  • Formāts: EPUB+DRM
  • Izdošanas datums: 12-Sep-2016
  • Izdevniecība: Academic Press Inc
  • Valoda: eng
  • ISBN-13: 9780128113127
Citas grāmatas par šo tēmu:
  • Formāts - EPUB+DRM
  • Cena: 72,31 €*
  • * ši ir gala cena, t.i., netiek piemērotas nekādas papildus atlaides
  • Ielikt grozā
  • Pievienot vēlmju sarakstam
  • Šī e-grāmata paredzēta tikai personīgai lietošanai. E-grāmatas nav iespējams atgriezt un nauda par iegādātajām e-grāmatām netiek atmaksāta.
  • Formāts: EPUB+DRM
  • Izdošanas datums: 12-Sep-2016
  • Izdevniecība: Academic Press Inc
  • Valoda: eng
  • ISBN-13: 9780128113127
Citas grāmatas par šo tēmu:

DRM restrictions

  • Kopēšana (kopēt/ievietot):

    nav atļauts

  • Drukāšana:

    nav atļauts

  • Lietošana:

    Digitālo tiesību pārvaldība (Digital Rights Management (DRM))
    Izdevējs ir piegādājis šo grāmatu šifrētā veidā, kas nozīmē, ka jums ir jāinstalē bezmaksas programmatūra, lai to atbloķētu un lasītu. Lai lasītu šo e-grāmatu, jums ir jāizveido Adobe ID. Vairāk informācijas šeit. E-grāmatu var lasīt un lejupielādēt līdz 6 ierīcēm (vienam lietotājam ar vienu un to pašu Adobe ID).

    Nepieciešamā programmatūra
    Lai lasītu šo e-grāmatu mobilajā ierīcē (tālrunī vai planšetdatorā), jums būs jāinstalē šī bezmaksas lietotne: PocketBook Reader (iOS / Android)

    Lai lejupielādētu un lasītu šo e-grāmatu datorā vai Mac datorā, jums ir nepieciešamid Adobe Digital Editions (šī ir bezmaksas lietotne, kas īpaši izstrādāta e-grāmatām. Tā nav tas pats, kas Adobe Reader, kas, iespējams, jau ir jūsu datorā.)

    Jūs nevarat lasīt šo e-grāmatu, izmantojot Amazon Kindle.

Anticandidal Agents is apt for providing thorough information on Candida drug resistance and its remedial implications. With this compilation we provide a comprehensive view on overcoming resistance in anticandidal drugs along with information on novel molecules.

Candida albicans is an opportunistic pathogenic fungus responsible for life threating invasive and nosocomial infections across the globe. Candidiasis is a major cause of morbidity among immunocompromised patients. Infections caused by non-albicans Candida like C. glabrata, C. parapsilosis, C. tropicalis have also imposed a serious threat in the last few decades. Current treatment of candidiasis relies primarily on antifungal agents broadly categorized as azoles, polyenes, echinocandins, allylamines and pyrimidines. Lately antifungal resistance has emerged to be an obstruction of current treatment regime. A number of reasons are accountable for occurrence of resistance that is well described in detail. Understanding the mechanisms of resistance is crucial for developing strategies for overcoming the hindrance in current therapeutics. A eukaryotic fungal cell share significant similarity with human cells. Due to dearth of selective fungal targets, ineffective drugs and severity of infection there is ardent need of new antifungal agents. Incompetence of the existing treatment is evident by high mortality and morbidity patient data. Henceforth both new drug targets and new drug leads are equally needed. Moreover as compared to antibacterials that have developed over time; the growth of antifungals has always lagged behind. Therefore antifungal pipeline is evidently dry with resistance as its major barrier. A complete understanding of Candida resistance helps in therapeutic expansion by development of novel drugs.

  • A complete understanding of Candida resistance helps in therapeutic expansion by development of novel drugs
  • Provides thorough information on Candida drug resistance and its remedial implications
  • Understanding the mechanisms of resistance is crucial for developing strategies for overcoming the hindrance in current therapeutics

Papildus informācija

Provides a complete understanding of candida resistance that may help in developing novel drugs
List of Figures
vii
List of Tables
ix
Chapter 1 Introduction
1(6)
Pathogenesis and Virulence
2(1)
Genome and Proteome
3(1)
Genetics
4(1)
Metabolome
5(2)
Chapter 2 Host-Pathogen Interaction
7(4)
Morphogenesis
7(1)
Immune Responses
8(3)
Chapter 3 Antifungals Used Against Candidiasis
11(30)
Azoles
12(4)
Polyenes
16(3)
Echinocandins
19(3)
Allylamines
22(1)
Pyrimidines
23(1)
Thiocarbamates and Morpholines
24(1)
Other Inhibitors
25(2)
Novel Inhibitors
27(10)
Differential Expression of Genes in Response to Drugs
37(4)
Chapter 4 Drug Resistance in Candida
41(8)
Emergence of Drug Resistance
41(3)
Spread of Drug Resistance
44(1)
Persistence of Drug Resistance
45(2)
Multidrug Resistance
47(2)
Chapter 5 Multidrug Resistance and Transporters
49(6)
Overview of Efflux Pumps
49(4)
Fungal Efflux-Mediated Drug Resistance
53(1)
Overcoming Efflux-Mediated Drug Resistance
53(2)
Chapter 6 Potential Anticandidal Targets
55(8)
Surface Targets
55(1)
Key Factors
56(2)
Cellular Targets
58(2)
Cross Talk
60(3)
Chapter 7 Drug Development Strategies
63(10)
In Vitro Based
63(3)
In Vivo Based
66(3)
In Silico Based
69(4)
Chapter 8 Conclusion
73(2)
Abbreviations 75(2)
Bibliography 77
Dr. Awanish Kumar is currently an Associate Professor in the Department of Biotechnology at the National Institute of Technology, Raipur (CG), India. He has more than 13 years of research experience. He received his PhD in molecular parasitology from the CSIR-Central Drug Research Institute, Lucknow, India, and Jawaharlal Nehru University, Delhi, India, and completed his postdoctoral studies at McGill University, Montreal, Canada. His research interests are infection biology, drug targeting, and drug discovery. He has served on various national and international organizations in different academic and research capacities. He has also served on many national committees and scientific advisory panels, as a member of many international professional research societies, and as a reviewer and editorial board member of reputed and refereed journals. He has authored or edited several monographs, books, and book chapters.