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Related Concept Videos

Traumatic Brain Injury l: Introduction01:28

Traumatic Brain Injury l: Introduction

DefinitionTraumatic brain injury, or TBI, is a disturbance of normal brain function induced by an external mechanical force, such as a direct blow to the head or a penetrating injury. It can affect both brain structure and function, producing a wide range of clinical outcomes. TBI is a heterogeneous condition, meaning its effects may differ based on the type, location, and severity of the injury.Basis of ClassificationTBI is classified based on severity, injury mechanism, or pathophysiology. In...
Spinal Cord Injury ll: Pathophysiology01:14

Spinal Cord Injury ll: Pathophysiology

Spinal cord injury progresses through two interconnected phases: primary injury and secondary injury.Primary InjuryPrimary injury happens at the moment of trauma and involves immediate mechanical damage to the spinal cord.Compression happens when broken vertebrae, herniated discs, or accumulating blood (such as a hematoma) press directly against the spinal cord, distorting its normal shape and function. In cases of contusion, the cord is bruised by a blunt force (like penetrating injuries or...
Secondary Spinal Cord Injury llI: Pathophysiology01:25

Secondary Spinal Cord Injury llI: Pathophysiology

Early Ischemia and Ionic ImbalanceWithin minutes of spinal cord injury, a secondary cascade begins, progressing over hours to weeks. Vascular damage reduces blood flow, causing ischemia and mitochondrial dysfunction. ATP depletion leads to ion pump failure, membrane depolarization, sodium influx, potassium efflux, and water accumulation, resulting in cellular swelling. Increased intracellular calcium further disrupts mitochondria and accelerates cellular injury.Excitotoxicity and Neuronal...
Increased Intracranial Pressure ll: Pathophysiology01:29

Increased Intracranial Pressure ll: Pathophysiology

Increased intracranial pressure (ICP) refers to a potentially life-threatening rise in pressure inside the skull. This usually happens when there is a major change in the volume of brain tissue, blood, or cerebrospinal fluid (CSF) — the three components inside the skull. According to the Monro-Kellie doctrine, if the volume of one component increases, the volumes of the other components must decrease to maintain normal pressure. If this does not happen, ICP rises.The process often begins with...

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Related Experiment Video

Updated: Jul 17, 2026

Controlled Cortical Impact Model for Traumatic Brain Injury
05:30

Controlled Cortical Impact Model for Traumatic Brain Injury

Published on: August 5, 2014

Activin A in brain injury.

Pasquale Florio1, Diego Gazzolo, Stefano Luisi

  • 1Department of Pediatrics, Obstetrics and Reproductive Medicine, University of Siena, Siena, Italy.

Advances in Clinical Chemistry
|January 26, 2007
PubMed
Summary

Activin A, a TGF-beta superfamily protein, is upregulated after acute brain injury. Its measurement may serve as a biomarker for detecting, locating, and predicting the extent of brain damage.

Area of Science:

  • Neuroscience
  • Molecular Biology
  • Biochemistry

Background:

  • Activin A is a dimeric protein within the transforming growth factor beta (TGF-beta) superfamily.
  • Its biological activity is regulated by specific receptors and binding proteins like follistatin.
  • Activin A, its receptors, and binding proteins are widely expressed in the brain.

Purpose of the Study:

  • To investigate the role of Activin A in acute brain injury.
  • To explore the potential of Activin A as a biomarker for brain damage.
  • To assess the neuroprotective effects of Activin A.

Main Methods:

  • Studies utilized models of acute brain injury (hypoxic/ischemic, mechanical, chemical).
  • Examined the expression levels of Activin A in response to neuronal damage.

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Controlled Cortical Impact Model of Mouse Brain Injury with Therapeutic Transplantation of Human Induced Pluripotent Stem Cell-Derived Neural Cells
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Controlled Cortical Impact Model of Mouse Brain Injury with Therapeutic Transplantation of Human Induced Pluripotent Stem Cell-Derived Neural Cells

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Stereotactic Atlas-Guided Laser Capture Microdissection of Brain Regions Affected by Traumatic Injury
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Stereotactic Atlas-Guided Laser Capture Microdissection of Brain Regions Affected by Traumatic Injury

Published on: September 11, 2017

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Last Updated: Jul 17, 2026

Controlled Cortical Impact Model for Traumatic Brain Injury
05:30

Controlled Cortical Impact Model for Traumatic Brain Injury

Published on: August 5, 2014

Controlled Cortical Impact Model of Mouse Brain Injury with Therapeutic Transplantation of Human Induced Pluripotent Stem Cell-Derived Neural Cells
09:29

Controlled Cortical Impact Model of Mouse Brain Injury with Therapeutic Transplantation of Human Induced Pluripotent Stem Cell-Derived Neural Cells

Published on: July 10, 2019

Stereotactic Atlas-Guided Laser Capture Microdissection of Brain Regions Affected by Traumatic Injury
09:29

Stereotactic Atlas-Guided Laser Capture Microdissection of Brain Regions Affected by Traumatic Injury

Published on: September 11, 2017

  • Investigated the downstream pathways activated by Activin A.
  • Main Results:

    • Acute brain injury strongly upregulates Activin A expression.
    • Activin A demonstrates robust neuroprotective activities and aids neuronal recovery.
    • Early induction of Activin A correlates with the presence and extent of brain injury.

    Conclusions:

    • Activin A is a key mediator in the brain's response to acute injury.
    • Measuring Activin A levels can serve as a biochemical index for brain damage.
    • This biomarker approach may aid in diagnosing subclinical lesions and establishing prognosis.