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

Oxidation of Phenols to Quinones01:17

Oxidation of Phenols to Quinones

In the presence of oxidizing agents, phenols are oxidized to quinones. Quinones can be easily reduced back to phenols using mild reducing agents. The electron-donating hydroxyl group enhances the reactivity of the aromatic ring, enabling oxidation of the ring even in the absence of an α hydrogen.
o-hydroxy phenols are oxidized to o-quinones and p-hydroxy phenols to p-quinones. Such redox reactions involve the transfer of two electrons and two protons. The reversible redox property is crucial in...
Cerebral Edema l: Introduction01:19

Cerebral Edema l: Introduction

Cerebral edema is a pathological increase in brain water content that disrupts intracranial pressure regulation and impairs neurological function. Because the cranial vault is rigid, even modest increases in tissue volume can compromise cerebral perfusion, distort neural structures, and initiate secondary injury. Cerebral edema develops through four principal mechanisms: vasogenic, cytotoxic, interstitial, and ionic.Vasogenic EdemaVasogenic edema arises from disruption of the blood–brain...
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...
Glaucoma: Overview01:25

Glaucoma: Overview

Glaucoma is an eye condition characterized by increased intraocular pressure that damages the retina and optic nerve, leading to irreversible blindness if left untreated. The human eye has various components, including the cornea, iris, pupil, lens, and optic nerve. Aqueous humor is secreted by the epithelium of the ciliary body in the posterior chamber and flows through the trabecular meshwork and canal of Schlemm, maintaining normal intraocular pressure. The trabecular meshwork and the canal...
Open Angle Glaucoma: Treatment01:27

Open Angle Glaucoma: Treatment

In open-angle glaucoma, the iridocorneal angle remains open, but the trabecular meshwork becomes stiff, slowing down the outflow of aqueous humor. This causes a buildup of aqueous humor in the anterior chamber, leading to a sudden increase in intraocular pressure. The treatment for open-angle glaucoma focuses on reducing the elevated intraocular pressure by either decreasing the secretion of aqueous humor or increasing its outflow.
Drugs such as carbonic anhydrase inhibitors, α2- and...
Pulmonary Edema II: Pathophysiology01:18

Pulmonary Edema II: Pathophysiology

Pulmonary edema is the accumulation of fluid in the interstitial and alveolar spaces of the lungs, impairing gas exchange and oxygen delivery. It may be cardiogenic or noncardiogenic, but both reduce oxygenation and lung compliance.Cardiogenic Pulmonary EdemaCardiogenic edema results from increased hydrostatic pressure in pulmonary capillaries, usually due to left ventricular dysfunction from myocardial infarction, heart failure, or valvular disease. Ineffective cardiac pumping causes blood to...

You might also read

Related Articles

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

Sort by
Same author

Domenico Mistichelli (1675-1717).

Journal of neurology·2025
Same author

The history of the European Neurological Society (1986-2014)-10 years later.

European journal of neurology·2024
Same author

Pioneers in neurology: a silver anniversary perspective.

Journal of neurology·2024
Same author

A (delayed) history of the brain lymphatic system.

Nature medicine·2019
Same author

[Are mental and neurological disorders related?]

Nederlands tijdschrift voor geneeskunde·2019
Same author

Macdonald Critchley (1900-1997).

Journal of neurology·2017

Related Experiment Video

Updated: May 18, 2026

Fluorescence-quenching of a Liposomal-encapsulated Near-infrared Fluorophore as a Tool for In Vivo Optical Imaging
10:55

Fluorescence-quenching of a Liposomal-encapsulated Near-infrared Fluorophore as a Tool for In Vivo Optical Imaging

Published on: January 5, 2015

[Quincke and his oedema].

Jan van Gijn1, Joost P Gijselhart

  • 1Nederlands Tijdschrift voor Geneeskunde, Amsterdam, the Netherlands. jan@vangijn.com

Nederlands Tijdschrift Voor Geneeskunde
|September 27, 2012
PubMed
Summary

Heinrich Quincke described hereditary angioedema, noting its association with increased vascular permeability. His work laid the foundation for understanding this rare condition, though he incorrectly attributed it to neurogenic factors.

Area of Science:

  • Medicine
  • Dermatology
  • Genetics

Background:

  • Heinrich Irenaeus Quincke (1842-1922) was a pivotal figure in internal medicine and clinical observation.
  • He completed his medical studies in Berlin and trained under Von Frerichs, later holding professorships in Berne and Kiel.
  • Quincke's career spanned significant advancements in medical understanding and practice.

Discussion:

  • In 1882, Quincke detailed 'acute, circumscribed oedema of the skin,' now recognized as hereditary angioedema (HAE).
  • He accurately identified increased vascular permeability as a key feature and differentiated familial from sporadic cases.
  • Quincke's hypothesis on neurogenic causes contrasts with current understanding of bradykinin pathway dysregulation.

Key Insights:

  • Quincke's meticulous clinical descriptions of hereditary angioedema remain foundational.

More Related Videos

Application of Acupotomy in a Knee Osteoarthritis Model in Rabbit
08:40

Application of Acupotomy in a Knee Osteoarthritis Model in Rabbit

Published on: October 20, 2023

Invasive Hemodynamic Characterization of the Portal-hypertensive Syndrome in Cirrhotic Rats
09:37

Invasive Hemodynamic Characterization of the Portal-hypertensive Syndrome in Cirrhotic Rats

Published on: August 1, 2018

Related Experiment Videos

Last Updated: May 18, 2026

Fluorescence-quenching of a Liposomal-encapsulated Near-infrared Fluorophore as a Tool for In Vivo Optical Imaging
10:55

Fluorescence-quenching of a Liposomal-encapsulated Near-infrared Fluorophore as a Tool for In Vivo Optical Imaging

Published on: January 5, 2015

Application of Acupotomy in a Knee Osteoarthritis Model in Rabbit
08:40

Application of Acupotomy in a Knee Osteoarthritis Model in Rabbit

Published on: October 20, 2023

Invasive Hemodynamic Characterization of the Portal-hypertensive Syndrome in Cirrhotic Rats
09:37

Invasive Hemodynamic Characterization of the Portal-hypertensive Syndrome in Cirrhotic Rats

Published on: August 1, 2018

  • His work highlighted the importance of vascular permeability in the condition's pathophysiology.
  • He pioneered the lumbar puncture technique, initially for therapeutic purposes in hydrocephalus.
  • Outlook:

    • Further research into the humoral factors, such as C1-esterase inhibitor deficiency, has elucidated the genetic basis of HAE.
    • Modern understanding has shifted from Quincke's neurogenic hypothesis to the bradykinin pathway.
    • Quincke's legacy endures through his contributions to both HAE and neuro-diagnostic procedures.