東華大學圖書館 |

語系: 繁體中文

說明(常見問題)

回圖書館首頁

手機版館藏查詢

登入

回首頁

切換: 標籤 | MARC模式 | ISBD

What doesn't kill you makes you stro...

Iffland, Philip H., II.

FindBook

Google Book

Amazon

博客來

What doesn't kill you makes you stronger: The paradoxical effect of antibodies in epilepsy.

紀錄類型:	書目-電子資源 : Monograph/item
正題名/作者:	What doesn't kill you makes you stronger: The paradoxical effect of antibodies in epilepsy./
作者:	Iffland, Philip H., II.
出版者:	Ann Arbor : ProQuest Dissertations & Theses, : 2015,
面頁冊數:	208 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=3718262
ISBN:	9781321980448

What doesn't kill you makes you stronger: The paradoxical effect of antibodies in epilepsy.
Iffland, Philip H., II.

What doesn't kill you makes you stronger: The paradoxical effect of antibodies in epilepsy. - Ann Arbor : ProQuest Dissertations & Theses, 2015 - 208 p.

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

Thesis (Ph.D.)--Kent State University, 2015.

Many types of epilepsy, autoimmune or otherwise, are associated with the presence of autoantibodies against neuronal proteins. Paradoxically, antibodies (IVIg) have also been used to treat epilepsy. The goals of this research were twofold: 1) Determine the CNS location of antibodies in patients with non-autoimmune epilepsies and the targets of these antibodies; and 2) Examine the effects of endogenous and exogenous specific and non-specific antibodies in two status epilepticus (SE) models.

ISBN: 9781321980448Subjects--Topical Terms:

3172791
Cellular biology.

What doesn't kill you makes you stronger: The paradoxical effect of antibodies in epilepsy.
LDR:03500nmm a2200397 4500 001 2153587
005 20171130090823.5
008 190424s2015 ||||||||||||||||| ||eng d
020 $a 9781321980448
035 $a (MiAaPQ)AAI3718262
035 $a AAI3718262
040 $a MiAaPQ $c MiAaPQ
100 1 $a Iffland, Philip H., II. $3 3341320
245 1 0 $a What doesn't kill you makes you stronger: The paradoxical effect of antibodies in epilepsy.
260 1 $a Ann Arbor : $b ProQuest Dissertations & Theses, $c 2015
300 $a 208 p.
500 $a Source: Dissertation Abstracts International, Volume: 77-01(E), Section: B.
500 $a Adviser: Derek S. Damron.
502 $a Thesis (Ph.D.)--Kent State University, 2015.
520 $a Many types of epilepsy, autoimmune or otherwise, are associated with the presence of autoantibodies against neuronal proteins. Paradoxically, antibodies (IVIg) have also been used to treat epilepsy. The goals of this research were twofold: 1) Determine the CNS location of antibodies in patients with non-autoimmune epilepsies and the targets of these antibodies; and 2) Examine the effects of endogenous and exogenous specific and non-specific antibodies in two status epilepticus (SE) models.
520 $a Immunohistochemistry and Western blotting were used to localize antibodies in patients with epilepsy, multiple sclerosis (MS) and arteriovenous malformation. Further analysis by ELISA, HEp-2 assay and immunoprecipitation revealed antibody targets. In mouse model experiments, lupus-prone or C57B6/J mice were injected with pilocarpine or kainic acid and monitored by EEG. Mice were treated with IV or IP injection of native or denatured IgGs, at time of or 12 hours before chemoconvulsant. Tissues were processed for immunohistochemistry and ELISA.
520 $a Brain regions from patients with epilepsy contained extravasated IgGs. Intracellular antibodies were found in epilepsy but not in MS brain. In brain from patients with epilepsy, only neurons displayed nuclear IgGs. All subcellular fractions from brain resections of patients with epilepsy contained extravasated IgGs. In the nuclear IgG pool, anti-histone autoantibodies were identified by two independent methods. Serum analysis revealed anti-histone and anti-chromatin antibodies only in patients with epilepsy.
520 $a In lupus-prone mice elevated serum IgGs favored post-SE survival. C57B6/J mice injected with native rat IgGs displayed a 40% reduction in pilocarpine-SE compared to control. IgGs extravasated in brains of untreated SE mice, but IgG-treated mice, with no pilocarpine-SE, experienced no parenchymal accumulation of IgGs. IgG leakage was observed in brain samples from KA treated mice and IgG treatment was largely ineffective.
520 $a These results show intracellular IgGs in brain of patients with epilepsy are targeted to histones and chromatin. Further, injected non-specific IgGs have a seizure mitigating effect prophylactically or acutely. Intact IgGs prevent blood-brain barrier leakage and SE and may exert their effect on peripheral inflammation. As rat IgGs were used in these experiments, IVIg may exert its effect through a non-Fc receptor mechanism.
590 $a School code: 0101.
650 4 $a Cellular biology. $3 3172791
650 4 $a Medicine. $3 641104
650 4 $a Neurobiology. $3 588707
650 4 $a Biomedical engineering. $3 535387
650 4 $a Immunology. $3 611031
650 4 $a Neurosciences. $3 588700
650 4 $a Biology. $3 522710
690 $a 0379
690 $a 0564
690 $a 0421
690 $a 0541
690 $a 0982
690 $a 0317
690 $a 0306
710 2 $a Kent State University. $b Biomedical Sciences. $3 3341321
773 0 $t Dissertation Abstracts International $g 77-01B(E).
790 $a 0101
791 $a Ph.D.
792 $a 2015
793 $a English
856 4 0 $u http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=3718262