語系:
繁體中文
English
說明(常見問題)
登入
回首頁
切換:
標籤
|
MARC模式
|
ISBD
Studies of pathological dynamics aft...
~
Rosidi, Nathanael L.
Studies of pathological dynamics after microvascular injury using nonlinear optical methods.
紀錄類型:
書目-語言資料,印刷品 : Monograph/item
正題名/作者:
Studies of pathological dynamics after microvascular injury using nonlinear optical methods./
作者:
Rosidi, Nathanael L.
面頁冊數:
225 p.
附註:
Source: Dissertation Abstracts International, Volume: 73-02, Section: B, page: 1089.
Contained By:
Dissertation Abstracts International73-02B.
標題:
Biology, Neurobiology. -
電子資源:
http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=3485169
ISBN:
9781267017192
Studies of pathological dynamics after microvascular injury using nonlinear optical methods.
Rosidi, Nathanael L.
Studies of pathological dynamics after microvascular injury using nonlinear optical methods.
- 225 p.
Source: Dissertation Abstracts International, Volume: 73-02, Section: B, page: 1089.
Thesis (Ph.D.)--Cornell University, 2011.
Microvascular lesions are a common feature in the aging brain and clinical evidence has correlated microvascular pathology with the development of neurodegenerative diseases such as Alzheimer's disease and dementia. Traditional animal models that replicate hemorrhagic and ischemic lesions in the brain typically affect large regions in the cortex and do not reproduce the small-scale lesions linked to neurodegeneration that likely stem from injuries to single microvessels. Due in part to this lack of small-scale injury animal models, there remains an incomplete understanding of the cellular and pathophysiological dynamics following small-scale vascular lesions, making progress on therapeutic strategies difficult. We used tightly focused femtosecond laser pulses to injure single penetrating arterioles (PA) (i.e., arterioles that plunge into the brain) in the cortex of live anesthetized rodents and used two-photon excited fluorescence (2PEF) imaging to quantify blood flow changes and to determine the time course of pathological consequences in the brain after injury.
ISBN: 9781267017192Subjects--Topical Terms:
845493
Biology, Neurobiology.
Studies of pathological dynamics after microvascular injury using nonlinear optical methods.
LDR
:04321nam 2200325 4500
001
712961
005
20121003100317.5
008
121101s2011 ||||||||||||||||| ||eng d
020
$a
9781267017192
035
$a
(UMI)AAI3485169
035
$a
AAI3485169
040
$a
UMI
$c
UMI
100
1
$a
Rosidi, Nathanael L.
$3
845491
245
1 0
$a
Studies of pathological dynamics after microvascular injury using nonlinear optical methods.
300
$a
225 p.
500
$a
Source: Dissertation Abstracts International, Volume: 73-02, Section: B, page: 1089.
500
$a
Adviser: Chris Schaffer.
502
$a
Thesis (Ph.D.)--Cornell University, 2011.
520
$a
Microvascular lesions are a common feature in the aging brain and clinical evidence has correlated microvascular pathology with the development of neurodegenerative diseases such as Alzheimer's disease and dementia. Traditional animal models that replicate hemorrhagic and ischemic lesions in the brain typically affect large regions in the cortex and do not reproduce the small-scale lesions linked to neurodegeneration that likely stem from injuries to single microvessels. Due in part to this lack of small-scale injury animal models, there remains an incomplete understanding of the cellular and pathophysiological dynamics following small-scale vascular lesions, making progress on therapeutic strategies difficult. We used tightly focused femtosecond laser pulses to injure single penetrating arterioles (PA) (i.e., arterioles that plunge into the brain) in the cortex of live anesthetized rodents and used two-photon excited fluorescence (2PEF) imaging to quantify blood flow changes and to determine the time course of pathological consequences in the brain after injury.
520
$a
We find that after ischemic occlusion of a PA, nearby pial and penetrating arterioles do not actively compensate for the reduction of blood flow observed near the occluded blood vessel. We find that capillaries connected downstream to the clotted vessel dilate but other capillaries in the vicinity do not, suggesting that any compensatory signal that results in a physiological response travels vascularly.
520
$a
We ruptured individual PAs to induce microhemorrhages that resulted in extravasation of blood into the parenchyma. We find that tissue compression due to the hematoma does not collapse capillaries and cause acute ischemia. 2PEF imaging of mice expressing yellow fluorescent protein (YFP) in a subset of cortical neurons revealed no dendrite degeneration out to seven days after microhemorrhage. However, we did observe an inflammatory response by microglia/macrophages as quickly as 1.5-hrs after microhemorrhage which persisted past seven days. Lastly, we looked at spine (i.e., post-synaptic terminals on dendrites) dynamics on GFP fluorescent cortical dendrites and found a higher rate of spine loss and gain after a nearby microhemorrhage out to 14 days. This higher rate of spine turnover may help provide an understanding of the development of symptomatic dysfunction due to consequences in neuronal rewiring after a microhemorrhage.
520
$a
The work presented in this dissertation provides quantification of pathological consequences after both ischemic and hemorrhagic injury to a single blood vessel in the brain. We see that after a small-scale ischemic lesion, surrounding blood vessels do not elicit an active response to compensate for a lack of blood flow in the targeted blood vessel and surrounding tissue. After a hemorrhage to a single blood vessel, we do not observe any neuronal degeneration or death. These hemorrhagic lesions, however, do result in an inflammatory reaction that may lead to subtle changes in neuronal rewiring or seed the development of neurodegenerative diseases. The work presented in this dissertation can help provide new insights for the development of novel stroke therapeutics as well as provide cell specific observations about the development of pathological consequences in both ischemic and hemorrhagic lesions in the brain.
590
$a
School code: 0058.
650
4
$a
Biology, Neurobiology.
$3
845493
650
4
$a
Engineering, Biomedical.
$3
845403
650
4
$a
Physics, Optics.
$3
845404
690
$a
0421
690
$a
0541
690
$a
0752
710
2
$a
Cornell University.
$3
845492
773
0
$t
Dissertation Abstracts International
$g
73-02B.
790
1 0
$a
Schaffer, Chris,
$e
advisor
790
$a
0058
791
$a
Ph.D.
792
$a
2011
856
4 0
$u
http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=3485169
筆 0 讀者評論
多媒體
評論
新增評論
分享你的心得
Export
取書館別
處理中
...
變更密碼[密碼必須為2種組合(英文和數字)及長度為10碼以上]
登入