Aida Maddahi
1 – 10 of 20
- show: 10
- |
- sort: year (new to old)
Close
Embed this list
<iframe src=" "
width=" "
height=" "
allowtransparency="true"
frameborder="0">
</iframe>
- 2017
-
Mark
C1-inactivator is upregulated in glioblastoma
(
- Contribution to journal › Article
- 2014
-
Mark
Plasticity of Cerebrovascular Smooth Muscle Cells After Subarachnoid Hemorrhage
(
- Contribution to journal › Article
- 2013
-
Mark
VIP/PACAP receptors in cerebral arteries of rat: Characterization, localization and relation to intracellular calcium.
(
- Contribution to journal › Article
- 2012
-
Mark
MAPK and pro-inflammatory mediators in the walls of brain blood vessels following cerebral ischemia
(
- Thesis › Doctoral thesis (compilation)
-
Mark
Regulation of enhanced cerebrovascular expression of proinflammatory mediators in experimental subarachnoid hemorrhage via the mitogen-activated protein kinase kinase/extracellular signal-regulated kinase pathway
(
- Contribution to journal › Article
- 2011
-
Mark
Inhibition of cerebrovascular raf activation attenuates cerebral blood flow and prevents upregulation of contractile receptors after subarachnoid hemorrhage
(
- Contribution to journal › Article
-
Mark
The role of tumor necrosis factor-alpha and TNF-alpha receptors in cerebral arteries following cerebral ischemia in rat
(
- Contribution to journal › Article
-
Mark
Blockade of the MEK/ERK pathway with a raf inhibitor prevents activation of pro-inflammatory mediators in cerebral arteries and reduction in cerebral blood flow after subarachnoid hemorrhage in a rat model.
2011) In Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism May 4. p.144-154(
- Contribution to journal › Article
- 2010
-
Mark
Subarachnoid Hemorrhage Induces Enhanced Expression of Thromboxane A(2) Receptors in Rat Cerebral Arteries.
(
- Contribution to journal › Article
-
Mark
Cerebral ischemia induces microvascular pro-inflammatory cytokine expression via the MEK/ERK pathway.
(
- Contribution to journal › Article