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Alternative targets for the treatmen...

Ajmo, Craig T., Jr.

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Alternative targets for the treatment of stroke.

紀錄類型:	書目-語言資料,印刷品 : Monograph/item
正題名/作者:	Alternative targets for the treatment of stroke./
作者:	Ajmo, Craig T., Jr.
面頁冊數:	198 p.
附註:	Adviser: Keith R. Pennypacker.
Contained By:	Dissertation Abstracts International68-12B.
標題:	Health Sciences, Pharmacology. -
電子資源:	http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=3292533
ISBN:	9780549359869

Alternative targets for the treatment of stroke.
Ajmo, Craig T., Jr.

Alternative targets for the treatment of stroke. - 198 p.

Adviser: Keith R. Pennypacker.

Thesis (Ph.D.)--University of South Florida, 2007.

Stroke is cerebrovascular injury that has been reported to be the third leading cause of death and the first leading cause of disability in the world (W. H. O. 2007). Currently, there is only one FDA approved treatment for stroke which is recombinant tissue plasminogen activator. This treatment has a narrow therapeutic window of three hours after ischemic stroke and can adversely cause the production of oxygen free radicals and intracranial hemorrhage. These limitations result in only 2-3% of all stroke victims as being candidates for this therapy as many patients do not arrive at the hospital in time to receive treatment, are not properly diagnosed, or do not know that they have had a stroke within this three hour time period. The purpose of these experiments was to elucidate alternative targets of stroke for the benefit of developing new treatments that stimulate neuroprotective and anti-inflammatory effects at the site of injury. It has been shown that transfusion of human umbilical cord blood cells up to 48 hours after stroke significantly reduces infarction and we have examined other targets that mimic these effects. We have shown that sigma receptor activation by DTG, a high affinity universal sigma agonist, reduces infarct volume when administered 24 hours after stroke. This suggests that modulation of neurodegenerative and inflammatory responses can extend the therapeutic window of treatment. For the first time, evidence is provided that shows that the spleen enhances the neurodegeneration caused by stroke as splenectomy prior to stroke profoundly decreased infarction volume. Finally, we studied signaling mechanisms of the splenic reaction to stroke and determined that this response is not directly dependent on neurotransmission via the splenic nerve. Denervation of the spleen prior to stroke showed no changes in neurodegenerative load at the site of injury in rat brains when compared to those subjected to stroke only. Overall, these experiments provide evidence showing that targets mediating neuroprotective and anti-inflammatory effects can lead to novel therapeutic interventions of stroke.

ISBN: 9780549359869Subjects--Topical Terms:

1017717
Health Sciences, Pharmacology.

Alternative targets for the treatment of stroke.
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