Stroke Core Targeting
Stroke Core Targeting - Related Videos
04:32
Exertional Heat Stroke Mouse Model: A Protocol to Study Mechanisms Underlying Exertional Heat Stroke
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2025
In this video we describe a step-by-step protocol to study exertional heat stroke (EHS) in a mouse model.
02:10
The Nucleosome Core Particle
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2020
Nucleosomes are the DNA-histone complex, where the DNA strand is wound around the histone core. The histone core is an octamer containing two copies of H2A, H2B, H3, and H4 histone proteins. The paradox Nucleosomes, paradoxically, perform two opposite functions simultaneously. On the one hand, their main responsibility is to protect the delicate DNA strands from physical damage and help achieve a higher compaction ratio. While on the other hand, they must allow polymerase enzymes to access DNA...
02:59
Stereotactic Injection of Hydrogel into a Post-Stroke Mouse Model
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2025
Source: Wilson, K.L., et al. Injection of Hydrogel Biomaterial Scaffolds to The Brain After Stroke. J. Vis. Exp. (2020)This video demonstrates the stereotaxic injection of a hydrogel into the stroke core of a post-stroke mouse, highlighting its role in scaffold formation that mimics the extracellular matrix, promotes cellular infiltration, and supports angiogenesis, underscoring its neurotherapeutic potential in stroke recovery.
02:23
Visualizing the Effect of pH on Solubilization of the Influenza A Viral Core
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2026
Source: Stauffer, S. et al., In Vitro Disassembly of Influenza A Virus Capsids by Gradient Centrifugation. J. Vis. Exp. (2016)This video demonstrates the effect of pH on the solubilization of influenza A viral cores. Gel electrophoresis and protein staining reveal the progressive disassembly of the core structure under acidic conditions.
08:14
Modeling Stroke in Mice: Permanent Coagulation of the Distal Middle Cerebral Artery
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Cited by 104 •
2014
Various murine models of middle cerebral artery occlusion (MCAO) are widely used in experimental brain research. Here, we demonstrate the model of transcranial permanent distal MCAO which produces consistent cortical infarction of a size corresponding to damage imposed by the majority of human ischemic strokes.
FAQs
The infarct core undergoes a linked sequence of oxygen and glucose deprivation, ATP depletion, ion imbalance, excitotoxicity, and progressive cell death. These biological changes indicate tissue with irreversible injury, making the core an important reference for measuring lesion severity and examining how ischemic damage develops over time.
Imaging methods help separate the infarct core from the penumbra, which is potentially salvageable tissue surrounding the most severely damaged region. This distinction connects structural or functional lesion assessment with treatment selection, allowing researchers to investigate whether an intervention limits tissue loss beyond the established core.
The two regions represent different biological conditions: the core has sustained irreversible injury, whereas the penumbra may remain viable. Directing strategies according to this contrast helps researchers evaluate whether treatment preserves threatened tissue, rather than simply documenting damage that has already become permanent.
Interpretation should account for the progression from energy failure to ion imbalance, excitotoxicity, and cell death. These processes explain why the core serves as a marker of severe ischemic injury and provide biological context for studying infarct evolution, comparing lesion assessments, and evaluating neuroprotective effects.
A study can first use imaging to identify the infarct core and distinguish it from the penumbra. Researchers then direct diagnostic or therapeutic strategies toward the relevant region, assess lesion extent or progression, and compare outcomes with the intended intervention. This workflow links anatomical targeting with treatment evaluation.
The approach supports lesion assessment, treatment selection, focused drug delivery, and evaluation of neuroprotective interventions. It is useful when a study must relate a strategy to the location and severity of ischemic injury, or when researchers need to determine whether an intervention limits infarct expansion and associated tissue loss.
Researchers can use the identified core as a reference for examining infarct evolution and judging whether a neuroprotective intervention limits tissue loss. Comparing lesion status with treatment exposure may clarify how effectively a strategy protects threatened brain tissue and may support interpretation of potential functional outcome improvements.