Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Concept Videos

Hepatic Encephalopathy01:29

Hepatic Encephalopathy

DefinitionHepatic encephalopathy is a reversible neurologic syndrome that results from advanced liver dysfunction or portosystemic shunting. It leads to disturbances in cognition, behavior, and motor function due to the brain’s exposure to gut-derived toxins that the liver fails to detoxify.EtiologyThis condition develops either in the setting of acute fulminant hepatitis or progressively during chronic liver disease, such as cirrhosis and portal hypertension. Portosystemic shunting—including...
Encephalitis ll: Pathophysiology01:26

Encephalitis ll: Pathophysiology

Encephalitis is inflammation of the brain parenchyma caused by direct viral invasion or immune-mediated mechanisms triggered by infections or tumors. Both processes lead to neuronal injury, disrupted neurotransmission, and diverse neurological symptoms, often with overlapping clinical and pathological features.Autoimmune EncephalitisIn autoimmune encephalitis, antibodies target neuronal antigens on cell surfaces, synapses, or within neurons. A key example is anti-NMDAR encephalitis, which can...
Cerebral Edema ll: Pathophysiology01:22

Cerebral Edema ll: Pathophysiology

Vasogenic edema is a major form of cerebral edema characterized by abnormal accumulation of fluid in the brain’s extracellular space due to disruption of the blood–brain barrier (BBB). The BBB is a specialized structure composed of endothelial cells connected by tight junctions, supported by astrocytic endfeet and a basement membrane. Under normal conditions, it tightly regulates the movement of ions, proteins, and solutes between the bloodstream and brain parenchyma. When this barrier loses...
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...
Anticholinesterase Agents: Poisoning and Treatment01:26

Anticholinesterase Agents: Poisoning and Treatment

Anticholinesterases, also known as cholinesterase inhibitors, work by blocking the breakdown of acetylcholine, leading to its accumulation in the synaptic cleft. This accumulation indirectly enhances both muscarinic and nicotinic actions. These agents are classified as reversible or irreversible based on their mechanism of action.     
Irreversible agents form a strong bond with the cholinesterase enzyme, making it inactive. The breakdown of the phosphorylated enzyme is slower than the...
Acute Respiratory Failure-III01:30

Acute Respiratory Failure-III

Hypercapnic respiratory failure, also known as Type 2 or ventilatory respiratory failure, is a severe condition characterized by the body's inability to effectively remove carbon dioxide (CO2) from the bloodstream. It leads to an arterial CO2 pressure (PaCO2) exceeding 45 mmHg and a blood pH above 7.35. This situation indicates that the body's ventilatory demand, or the ventilation needed to maintain normal PaCO2 levels, surpasses its supply or the maximum gas flow achievable without causing...

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by
Same author

Fundamental Understanding of Oxidative Stability in Fluorinated Asymmetric Ethers for Li Batteries.

Angewandte Chemie (International ed. in English)·2026
Same author

Metal electrode potential diverges with ion additions.

Nature chemistry·2026
Same author

Distinct clinical course and poor outcomes of small bowel bleeding in acute hematochezia: a nationwide multicenter study.

Scientific reports·2026
Same author

Prerequisite of Oxygen Local Environment for Facile Proton Intercalation into Transition-Metal Oxides.

Journal of the American Chemical Society·2026
Same author

A Low-Concentration All-Phosphate Electrolyte for High-Voltage and High-Safety Lithium-Ion Batteries.

Advanced materials (Deerfield Beach, Fla.)·2025
Same author

Causal Relationship between Potential Shift and Molecular Structure in Concentrated Electrolytes.

The journal of physical chemistry. B·2025
Same journal

A Possible Case of Drug-induced ANCA-associated Vasculitis Associated with Mirabegron.

Internal medicine (Tokyo, Japan)·2026
Same journal

Microangiopathic Hemolytic Anemia Due to Disseminated Carcinomatosis of the Bone Marrow in Esophageal Adenocarcinoma.

Internal medicine (Tokyo, Japan)·2026
Same journal

Recurrent Sigmoid Diverticulitis Managed with Adjunctive Daiobotanpito: A Case Report.

Internal medicine (Tokyo, Japan)·2026
Same journal

Tracheobronchial mucormycosis.

Internal medicine (Tokyo, Japan)·2026
Same journal

A Case of Transient ACTH and Cortisol Suppression Caused by Dexamethasone Mouthwash during Immune Checkpoint Inhibitor Treatment.

Internal medicine (Tokyo, Japan)·2026
Same journal

Acute Spinal Calcium Pyrophosphate Dehydrate Deposition Disease.

Internal medicine (Tokyo, Japan)·2026
See all related articles

Related Experiment Video

Updated: Jul 4, 2026

Cerebral Ischemic Coma Model Induced by Modified Four-Vessel Occlusion
03:37

Cerebral Ischemic Coma Model Induced by Modified Four-Vessel Occlusion

Published on: July 5, 2024

Delayed encephalopathy after carbon monoxide intoxication

Yuu Yamazaki1, Atsuo Yamada

  • 1Department of Neurology, National Hospital Organization Kure Medical Center, Hiroshima. yuu-y@axel.ocn.ne.jp

Internal Medicine (Tokyo, Japan)
|June 4, 2008
PubMed
Summary

No abstract available in PubMed .

More Related Videos

Experimental Models to Study the Neuroprotection of Acidic Postconditioning Against Cerebral Ischemia
10:13

Experimental Models to Study the Neuroprotection of Acidic Postconditioning Against Cerebral Ischemia

Published on: July 31, 2017

Related Experiment Videos

Last Updated: Jul 4, 2026

Cerebral Ischemic Coma Model Induced by Modified Four-Vessel Occlusion
03:37

Cerebral Ischemic Coma Model Induced by Modified Four-Vessel Occlusion

Published on: July 5, 2024

Experimental Models to Study the Neuroprotection of Acidic Postconditioning Against Cerebral Ischemia
10:13

Experimental Models to Study the Neuroprotection of Acidic Postconditioning Against Cerebral Ischemia

Published on: July 31, 2017