Blood Injection Intracerebral Hemorrhage Mouse Model

2019 ◽  
pp. 293-302
Author(s):  
Ludmila Belayev
Keyword(s):  
Mouse Model ◽  
Intracerebral Hemorrhage ◽  
Blood Injection

Blood Injection Subarachnoid Hemorrhage Mouse Model

2009 ◽  
pp. 287-292
Author(s):  
Tarkan Calisaneller ◽  
Chih-Lung Lin ◽  
Naoya Ukita ◽  
Ryo Yoshimura ◽  
Yi Wang ◽  
...  
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Mouse Model ◽  
Blood Injection

scholarly journals Heat shock protein 70 upregulation by geldanamycin reduces brain injury in a mouse model of intracerebral hemorrhage

2010 ◽  
Vol 57 (7) ◽  
pp. 844-850 ◽  
Author(s):  
Anatol Manaenko ◽  
Nancy Fathali ◽  
Hank Chen ◽  
Hidenori Suzuki ◽  
Shammah Williams ◽  
...  
Keyword(s):  
Brain Injury ◽  
Heat Shock ◽  
Mouse Model ◽  
Heat Shock Protein ◽  
Intracerebral Hemorrhage ◽  
Heat Shock Protein 70

scholarly journals Autologous Blood Injection to Model Spontaneous Intracerebral Hemorrhage in Mice

10.3791/2618 ◽  
2011 ◽  
Author(s):  
Lauren H. Sansing ◽  
Scott E. Kasner ◽  
Louise McCullough ◽  
Puneet Agarwal ◽  
Frank A. Welsh ◽  
...  
Keyword(s):  
Intracerebral Hemorrhage ◽  
Autologous Blood ◽  
Spontaneous Intracerebral Hemorrhage ◽  
Autologous Blood Injection ◽  
Blood Injection

scholarly journals [125 I]IodoDPA-713 Binding to 18 kDa Translocator Protein (TSPO) in a Mouse Model of Intracerebral Hemorrhage: Implications for Neuroimaging

2018 ◽  
Vol 12 ◽  
Author(s):  
Frederick Bonsack ◽  
Catherine A. Foss ◽  
Ali S. Arbab ◽  
Cargill H. Alleyne ◽  
Martin G. Pomper ◽  
...  
Keyword(s):  
Mouse Model ◽  
Intracerebral Hemorrhage ◽  
Translocator Protein

scholarly journals Magnetic Resonance Imaging Reveals Significantly Increased Cerebral Blood Flow in the Hemoglobin E Mouse Model

Blood ◽  
2021 ◽  
Vol 138 (Supplement 1) ◽  
pp. 2034-2034
Author(s):  
Min-Hui Cui ◽  
Craig A Branch ◽  
Rhoda Elison Hirsch
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Mouse Model ◽  
Intracerebral Hemorrhage ◽  
Transgenic Mouse ◽  
Transgenic Mouse Model ◽  
Left Ventricular ◽  
Hemoglobin E ◽  
Significant Difference ◽  
Normal Background

Abstract Hemoglobin E (HbE) is the most common hemoglobin mutation world-wide. EE individuals exhibit a mild anemia as do those with β-thalassemia trait. A paradox arises with the combination of two relatively benign genes in HbE/β-thalassemia (HbE/β-thal) giving rise to highly morbid symptoms, anemia, growth retardation, developmental retardation, thalassemic bone type development, chronic leg ulcers (for a review, S Fucharoen and DJ Weatherall 2012) and often early mortality arising from cardiac failure (N Olivieri, Z Pakbaz et al. 2011). One approach to understanding the characteristics of HbE and this paradox was to generate a transgenic mouse model, expressing solely human HbE. This HbE mouse model exhibits a mild oxidative stress that parallels that observed in human EE individuals (QY Chen, EE Bouhassira et al. 2004, QY Chen, ME Fabry et al. 2012). These transgenic mice also exhibit mild cardiac dysfunction with depressed left ventricular contraction. We present here the first evidence of a significant increase in cerebral blood flow in the full knockout HbE (HbEKO) transgenic mouse model expressing solely human HbE compared to both the HbE+HbF (γ, gamma)-globin transgenic mouse, and the normal background C57 mouse. Cerebral blood flow is assessed non-invasively by MRI imaging. All protocols were approved by the Albert Einstein Institutional Animal Care and Use Committee. Comparing the HbEKO mouse (without human γ globin) to the C57 normal background mouse, a significant increase of over 20% in thalamus cerebral blood flow at baseline is observed (p=0.008). There is also an approximate 18% reduction in thalamus cerebral blood flow comparing HbE low γ mice to the full HbEKO (no γ) (p=0.011). Concomitant with these observations, no significant difference is observed comparing these low gamma HbE mice to the normal C57 background mouse (p=0.384). The goodness of the data is also seen in the relatively small variation in cerebral blood flow amongst the individual mice in each subset. These findings are of particular relevance to reports of neurologic symptoms, intracerebral hemorrhage, and brain infarct in HbE/β-thal patients (V Wong, YL Yu et al. 1990, S Das, S Dubey et al. 2019). In conclusion, these results suggest a direct role of HbE RBC initiating altered cerebral blood flow that when further complexed with β-thal could lead to intracerebral hemorrhage and other cerebral pathophysiology. The finding that the HbEKO mice with high HbF are not significantly different in cerebral blood flow from C57 mice may lend further support to therapeutic approaches enhancing the production of HbF in severe hemoglobinopathies, such as in sickle cell anemia, HbE/β-thal, and β-thal individuals. Disclosures No relevant conflicts of interest to declare.

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