Longitudinal monitoring of blood perfusion and brain tissue damage in photothrombotic ischemic stroke rat model

2019 ◽  
Author(s):  
Shanshan Yang ◽  
Kezhou Liu ◽  
Guoqing Weng ◽  
Zhihua Ding ◽  
Peng Li
Keyword(s):  
Ischemic Stroke ◽  
Brain Tissue ◽  
Rat Model ◽  
Tissue Damage ◽  
Blood Perfusion ◽  
Brain Tissue Damage

Piezosurgery prevents brain tissue damage: an experimental study on a new rat model

2011 ◽  
Vol 40 (8) ◽  
pp. 840-844 ◽  
Author(s):  
G. Pavlíková ◽  
R. Foltán ◽  
M. Burian ◽  
E. Horká ◽  
S. Adámek ◽  
...  
Keyword(s):  
Experimental Study ◽  
Brain Tissue ◽  
Rat Model ◽  
Tissue Damage ◽  
Brain Tissue Damage

scholarly journals Spreading depolarizations increase delayed brain injury in a rat model of subarachnoid hemorrhage

2015 ◽  
Vol 36 (7) ◽  
pp. 1224-1231 ◽  
Author(s):  
Arend M Hamming ◽  
Marieke JH Wermer ◽  
S Umesh Rudrapatna ◽  
Christian Lanier ◽  
Hine JA van Os ◽  
...  
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Brain Tissue ◽  
Rat Model ◽  
Tissue Damage ◽  
Tissue Injury ◽  
Delayed Cerebral Ischemia ◽  
Doppler Flowmetry ◽  
Lesion Growth ◽  
Brain Tissue Damage ◽  
The Right

Spreading depolarizations may contribute to delayed cerebral ischemia after aneurysmal subarachnoid hemorrhage, but the effect of spreading depolarizations on brain lesion progression after subarachnoid hemorrhage has not yet been assessed directly. Therefore, we tested the hypothesis that artificially induced spreading depolarizations increase brain tissue damage in a rat model of subarachnoid hemorrhage. Subarachnoid hemorrhage was induced by endovascular puncture of the right internal carotid bifurcation. After one day, brain tissue damage was measured with T2-weighted MRI, followed by application of 1 M KCl (SD group, N = 16) or saline (no-SD group, N = 16) to the right cortex. Cortical laser-Doppler flowmetry was performed to record spreading depolarizations. MRI was repeated on day 3, after which brains were extracted for assessment of subarachnoid hemorrhage severity and histological damage. 5.0 ± 2.7 spreading depolarizations were recorded in the SD group. Subarachnoid hemorrhage severity and mortality were similar between the SD and no-SD groups. Subarachnoid hemorrhage-induced brain lesions expanded between days 1 and 3. This lesion growth was larger in the SD group (241 ± 233 mm3) than in the no-SD group (29 ± 54 mm3) (p = 0.001). We conclude that induction of spreading depolarizations significantly advances lesion growth after experimental subarachnoid hemorrhage. Our study underscores the pathophysiological consequence of spreading depolarizations in the development of delayed cerebral tissue injury after subarachnoid hemorrhage.

scholarly journals Study of Morphofunctional Parameters of Blood Cells in Ischemic Stroke Using a Genome-wide Research

2021 ◽  
pp. 70-75
Author(s):  
Ulyana Viktorovna Matveeva ◽  
Malika Ruslanovna Askhanova ◽  
Shamsi Aisayevich Saydaev ◽  
Alina Said-Alvievna Bakasheva ◽  
Diana Magomedovna Nauruzova ◽  
...  
Keyword(s):  
Ischemic Stroke ◽  
Early Diagnosis ◽  
Brain Tissue ◽  
Tissue Damage ◽  
Blood Cells ◽  
Risk Of Death ◽  
Apolipoprotein Ciii ◽  
Genome Wide ◽  
A Genome ◽  
Brain Tissue Damage

Biomarkers can play many useful roles in modern neurology. Early diagnosis and immediate therapy are important factors for reducing the degree of brain tissue damage in ischemic stroke, reduces the risk of death from stroke. In the current study, apolipoprotein CIII (ApoCIII), a biomarker of ischemic stroke, was found.

scholarly journals GAMBARAN FAKTOR RISIKO PADA PENDERITA STROKE ISKEMIK YANG DIRAWAT INAP NEUROLOGI RSUP PROF. DR. R. D. KANDOU MANADO PERIODE JULI 2012 - JUNI 2013

e-CliniC ◽  
2015 ◽  
Vol 3 (1) ◽  
Author(s):  
Glen Y. C. R. Kabi ◽  
Rizal Tumewah ◽  
Mieke A. H. N. Kembuan
Keyword(s):  
Risk Factors ◽  
Blood Flow ◽  
Ischemic Stroke ◽  
Brain Tissue ◽  
Tissue Damage ◽  
Medical Records ◽  
Clinical Signs ◽  
Stroke Patients ◽  
Brain Tissue Damage ◽  
The Brain

Abstract: Ischemic stroke is a clinical sign of dysfunction or brain tissue damage caused by lack of blood flow to the brain that disrupts the need for blood and oxygen to the brain. WHO defines stroke as a rapidly developing clinical signs of focal brain due to interference (or global) with symptoms - that last for 24 hours or more- and can cause death without any other obvious cause other than vascular. This study aimed to obtain an overview of risk factors in ischemic stroke patients in the Inpatient Neurology Department of Prof. Dr. R. D. Kandou Hospital Manado period July 2012 - June 2013. Data were taken by collecting data of ischemic stroke patients medical records. There were 60 patients during that period. Patients affected by stroke were aged between 51 - 65 years and had histories of hypertension.Keywords: risk factors, ischemic stroke.Abstrak: Stroke iskemik adalah tanda klinis disfungsi atau kerusakan jaringan otak yang disebabkan kurangnya aliran darah ke otak sehingga mengganggu kebutuhan darah dan oksigen di otak. WHO mendefiniskan stroke merupakan suatu tanda klinis yang berkembang cepat akibat gangguan otak fokal (atau global) dengan gejala - gejala yang berlangsung selama 24 jam atau lebih dan dapat menyebabkan kematian tanpa adanya penyebab lain yang jelas selain vaskuler. Penelitian ini bertujuan untuk mendapatkan gambaran tentang faktor resiko pada pasien stroke iskemik di rawat inap Neurologi RSUP Prof. Dr. R. D. Kandou Manado periode Juli 2012 - Juni 2013. Penelitian dilakukan dengan cara mengumpulkan data pasien yang terkena stroke iskemik di bagian rekam medik RSUP Prof. Dr. R. D. Kandou Manado. Didapatkan 60 pasiem selama periode Juli 2012 – Juni 2013. Berdasarkan hasil yang didapat maka disimpulkan bahwa pasien yang sering terkena stroke adalah pasien yang berumur antara 51-65 tahun, dan pasien yang memiliki riwayat hipertensi.Kata kunci: faktor risiko, stroke iskemik

MR Spectroscopic Evaluation of Brain Tissue Damage After Treatment for Pediatric Brain Tumors

2009 ◽  
pp. 183-186 ◽  
Author(s):  
Sławomir Blamek ◽  
Dawid Larysz ◽  
Kornelia Ficek ◽  
Maria Sokół ◽  
Leszek Miszczyk ◽  
...  
Keyword(s):  
Brain Tumors ◽  
Brain Tissue ◽  
Tissue Damage ◽  
Pediatric Brain Tumors ◽  
Brain Tissue Damage ◽  
Pediatric Brain

MONOPHASIC BUT NOT BIPHASIC PULSES INDUCE BRAIN TISSUE DAMAGE DURING MONOPOLAR HIGH-FREQUENCY DEEP BRAIN STIMULATION

Neurosurgery ◽  
2009 ◽  
Vol 64 (1) ◽  
pp. 156-163 ◽  
Author(s):  
Brigitte Piallat ◽  
Stéphan Chabardès ◽  
Annaelle Devergnas ◽  
Napoleon Torres ◽  
Marjolaine Allain ◽  
...  
Keyword(s):  
Deep Brain Stimulation ◽  
Brain Tissue ◽  
Brain Stimulation ◽  
Tissue Damage ◽  
High Frequency ◽  
Brain Tissue Damage ◽  
Deep Brain

Localized Brain Tissue Cooling for Use During Intracranial Thrombectomy

2012 ◽  
Author(s):  
Thomas L. Merrill ◽  
Denise R. Merrill ◽  
Jennifer E. Akers
Keyword(s):  
Ischemic Stroke ◽  
Reperfusion Injury ◽  
Brain Tissue ◽  
Ischemic Injury ◽  
Blood Perfusion ◽  
Neuroprotective Agents ◽  
Tissue Necrosis ◽  
Stroke Treatment ◽  
Neurological Outcomes

The primary goal of current ischemic stroke treatment is quickly restoring blood perfusion. Recanalization is linked to improved neurological outcomes [1]. Resulting tissue necrosis, however, following a stroke has two causes: 1) ischemic injury and 2) reperfusion injury. Therefore, development of neuroprotective agents specifically beneficial against reperfusion injury are required.

scholarly journals Acetaldehyde Induces Cytotoxicity of SH-SY5Y Cells via Inhibition of Akt Activation and Induction of Oxidative Stress

2016 ◽  
Vol 2016 ◽  
pp. 1-9 ◽  
Author(s):  
Tingting Yan ◽  
Yan Zhao ◽  
Xia Zhang
Keyword(s):  
Oxidative Stress ◽  
Brain Tissue ◽  
Cognitive Dysfunction ◽  
Tissue Damage ◽  
Heavy Drinking ◽  
Mitogen Activated Protein Kinase ◽  
Toxic Metabolite ◽  
Excessive Alcohol Consumption ◽  
Brain Tissue Damage ◽  
Induced Apoptosis

Excessive alcohol consumption can lead to brain tissue damage and cognitive dysfunction. It has been shown that heavy drinking is associated with an earlier onset of neurodegenerative diseases such as Alzheimer’s disease. Acetaldehyde, the most toxic metabolite of ethanol, is speculated to mediate the brain tissue damage and cognitive dysfunction induced by the chronic excessive consumption of alcohol. However, the exact mechanisms by which acetaldehyde induces neurotoxicity are not totally understood. In this study, we investigated the cytotoxic effects of acetaldehyde in SH-SY5Y cells and found that acetaldehyde induced apoptosis of SH-SY5Y cells by downregulating the expression of antiapoptoticBcl-2andBcl-xLand upregulating the expression of proapoptoticBax. Acetaldehyde treatment led to a significant decrease in the levels of activated Akt and cyclic AMP-responsive element binding protein (CREB). In addition, acetaldehyde induced the activation of p38 mitogen-activated protein kinase (MAPK) while inhibiting the activation of extracellular signal-regulated kinases (ERKs, p44/p42MAPK). Meanwhile, acetaldehyde treatment caused an increase in the production of reactive oxygen species and elevated the oxidative stress in SH-SY5Y cells. Therefore, acetaldehyde induces cytotoxicity of SH-SY5Y cells via promotion of apoptotic signaling, inhibition of cell survival pathway, and induction of oxidative stress.

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