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Host-factor enhancement of therapy f...

Schump, Michael David.

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Host-factor enhancement of therapy for tuberculosis.

紀錄類型:	書目-電子資源 : Monograph/item
正題名/作者:	Host-factor enhancement of therapy for tuberculosis./
作者:	Schump, Michael David.
面頁冊數:	82 p.
附註:	Source: Dissertation Abstracts International, Volume: 77-01(E), Section: B.
Contained By:	Dissertation Abstracts International77-01B(E).
標題:	Cellular biology. -
電子資源:	http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=3720811
ISBN:	9781339019277

Host-factor enhancement of therapy for tuberculosis.
Schump, Michael David.

Host-factor enhancement of therapy for tuberculosis. - 82 p.

Source: Dissertation Abstracts International, Volume: 77-01(E), Section: B.

Thesis (Ph.D.)--University of California, Berkeley, 2015.

Tuberculosis (TB) is a disease of major public health importance and improvements to its treatment could greatly benefit efforts aimed at eliminating the disease. Current treatment options for TB are limited in effectiveness and have numerous fundamental failings due to the necessarily lengthy duration of therapy and toxicity of the antimicrobial drugs deployed, among other issues. The studies described herein where undertaken with the goal of developing adjunctive treatments or modifications of existing treatments which could improve the treatment course, outcome, or both for standard TB antimicrobial chemotherapy.

ISBN: 9781339019277Subjects--Topical Terms:

3172791
Cellular biology.

Host-factor enhancement of therapy for tuberculosis.
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245 1 0 $a Host-factor enhancement of therapy for tuberculosis.
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500 $a Source: Dissertation Abstracts International, Volume: 77-01(E), Section: B.
500 $a Adviser: Lee W. Riley.
502 $a Thesis (Ph.D.)--University of California, Berkeley, 2015.
520 $a Tuberculosis (TB) is a disease of major public health importance and improvements to its treatment could greatly benefit efforts aimed at eliminating the disease. Current treatment options for TB are limited in effectiveness and have numerous fundamental failings due to the necessarily lengthy duration of therapy and toxicity of the antimicrobial drugs deployed, among other issues. The studies described herein where undertaken with the goal of developing adjunctive treatments or modifications of existing treatments which could improve the treatment course, outcome, or both for standard TB antimicrobial chemotherapy.
520 $a Three areas of research are discussed beginning with adaptive immune augmentation through therapeutic vaccination, proceeding to investigations of innate immune adjuvant therapy and concluding with host environment mediated improvement of selectivity index of TB antimicrobial compounds.
520 $a A post-treatment, therapeutic vaccine was studied with the goal of developing a tool which could prevent relapse or reactivation disease. Though the project was a follow up to a study which demonstrated exceptional protection, the vaccine candidate did not demonstrate any detectable efficacy in three parallel murine infection experiments. Possible reasons and implications of this failure are discussed.
520 $a Because correlates of protection for adaptive immunity to TB are poorly understood and have not proven to be tractable for intervention, innate immune enhancement was investigated. Autophagy, a cell-intrinsic process with antimicrobial capabilities, was selected due to its well described tuberculocidal activity and pharmacologic manipulability. However, despite the apparent capacity of some test compounds to increase autophagic flux, none demonstrated robust restriction of mycobacterial growth in murine or human macrophages. That study did, however, lead to the serendipitous discovery that pH based drug partitioning can increase the selectivity index of antimicrobial drugs against M. tuberculosis inside cultured macrophages.
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