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

Open Angle Glaucoma: Treatment01:27

Open Angle Glaucoma: Treatment

969
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...
969
Angle Closure Glaucoma: Treatment01:28

Angle Closure Glaucoma: Treatment

1.2K
Angle-closure glaucoma, or closed-angle glaucoma, is an eye condition where the iris bulges out and blocks the iridocorneal angle, resulting in a buildup of aqueous humor and increased intraocular pressure. Immediate medical attention is necessary due to the sudden onset of symptoms. The treatment for angle-closure glaucoma includes short-term and long-term approaches. Short-term treatment involves using eye drops like pilocarpine to lower intraocular pressure by increasing aqueous humor...
1.2K
Glaucoma: Overview01:25

Glaucoma: Overview

1.3K
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...
1.3K
Contact Angle01:13

Contact Angle

18.3K
When a solid is dipped inside a liquid, the liquid surface becomes curved near the contact. For some solid–liquid interfaces, the liquid is pulled up along the solid, while for others, the liquid surface is convex or depressed near the solid surface. This phenomenon can be explained using the concept of cohesive and adhesive forces.
The adhesive force is the molecular force between molecules of different materials, that is, between the molecules of the solid and the liquid. The cohesive...
18.3K
Angle of Twist: Problem Solving01:13

Angle of Twist: Problem Solving

762
An electric motor applies a torque of 700 N·m to an aluminum shaft, triggering a stable rotation. Two pulleys, B and C, are subjected to torques of 300 N·m and 400 N·m, respectively. The modulus of rigidity is provided as 25 GPa. With the knowledge of the length and diameter of each segment, the twist angle between the two pulleys can be computed. First, a section cut is made between pulleys B and C, and the cut cross-section is analyzed using a free-body diagram. Given that the torque...
762
Design Example: Traverse Angle Computations01:25

Design Example: Traverse Angle Computations

315
Traverse angle computations are a critical component of surveying, used to compute the internal angles within a closed traverse. A traverse consists of a series of connected lines forming a closed loop, often used for land boundary delineation or mapping. Calculating the internal angles ensures accuracy in the traverse geometry and is essential for checking survey data integrity.The process begins with known azimuths and bearings of the traverse sides. Internal angles at each vertex are...
315

You might also read

Related Articles

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

Sort by
Same author

MMP9 Genotype and Systemic T-Cell Subsets Correlate With Structural and Functional Outcomes in Neovascular Age-Related Macular Degeneration.

Investigative ophthalmology & visual science·2026
Same author

FOXC1 Duplications-New Mutations and Clinical Features in an Old Glaucoma Gene.

JAMA ophthalmology·2026
Same author

Single-Cell Gene Expression and eQTL Analyses in the Human Retina, RPE, and Choroid in Macular Degeneration.

bioRxiv : the preprint server for biology·2026
Same author

Isolated Haab Striae Point to a Pressured Past.

American journal of ophthalmology·2025
Same author

Double Bubble Trouble: Dual Retinal Tamponade Agents in the Anterior Chamber.

Ophthalmology. Glaucoma·2025
Same author

A Multitrait Polygenic Risk Score for Open-Angle Glaucoma Stratifies Risk of Pigmentary Glaucoma in Pigment Dispersion Syndrome.

Ophthalmology. Glaucoma·2025

Related Experiment Video

Updated: Jan 23, 2026

Assessing Early Stage Open-Angle Glaucoma in Patients by Isolated-Check Visual Evoked Potential
07:11

Assessing Early Stage Open-Angle Glaucoma in Patients by Isolated-Check Visual Evoked Potential

Published on: May 25, 2020

6.8K

Mendelian genes in primary open angle glaucoma.

Nathan C Sears1, Erin A Boese1, Mathew A Miller1

  • 1Department of Ophthalmology and Visual Sciences, Carver College of Medicine, University of Iowa, Iowa City, IA, USA.

Experimental Eye Research
|June 26, 2019
PubMed
Summary
This summary is machine-generated.

Genetic mutations in MYOC, OPTN, and TBK1 are linked to primary open-angle glaucoma (POAG) and normal tension glaucoma. Understanding these genetic causes offers new therapeutic targets for glaucoma treatment.

More Related Videos

Using the Gene Pulser MXcell Electroporation System to Transfect Primary Cells with High Efficiency
12:55

Using the Gene Pulser MXcell Electroporation System to Transfect Primary Cells with High Efficiency

Published on: January 7, 2010

24.7K
Ultrasound Cyclo Plasty in Eyes with Glaucoma
05:05

Ultrasound Cyclo Plasty in Eyes with Glaucoma

Published on: January 26, 2018

12.7K

Related Experiment Videos

Last Updated: Jan 23, 2026

Assessing Early Stage Open-Angle Glaucoma in Patients by Isolated-Check Visual Evoked Potential
07:11

Assessing Early Stage Open-Angle Glaucoma in Patients by Isolated-Check Visual Evoked Potential

Published on: May 25, 2020

6.8K
Using the Gene Pulser MXcell Electroporation System to Transfect Primary Cells with High Efficiency
12:55

Using the Gene Pulser MXcell Electroporation System to Transfect Primary Cells with High Efficiency

Published on: January 7, 2010

24.7K
Ultrasound Cyclo Plasty in Eyes with Glaucoma
05:05

Ultrasound Cyclo Plasty in Eyes with Glaucoma

Published on: January 26, 2018

12.7K

Area of Science:

  • Ophthalmology
  • Genetics
  • Molecular Biology

Background:

  • Primary open-angle glaucoma (POAG) is a leading cause of irreversible blindness.
  • Glaucoma can be inherited as a Mendelian trait, suggesting specific gene mutations are involved.
  • Identifying genetic factors is crucial for understanding glaucoma pathogenesis.

Purpose of the Study:

  • To investigate the role of myocilin (MYOC), optineurin (OPTN), and TANK binding kinase 1 (TBK1) gene mutations in POAG.
  • To elucidate the molecular mechanisms underlying MYOC- and OPTN/TBK1-associated glaucoma.
  • To identify potential gene-directed therapeutic targets for glaucoma.

Main Methods:

  • Genetic analysis of patients with POAG and normal tension glaucoma.
  • Molecular studies on the functional consequences of identified gene mutations.
  • Investigation of cellular pathways affected by these mutations, including protein trafficking, endoplasmic reticulum stress, and autophagy.

Main Results:

  • Mutations in MYOC account for 3-4% of POAG cases with elevated intraocular pressure (IOP).
  • Mutations in OPTN, TBK1, and MYOC each account for approximately 1% of normal tension glaucoma (IOP ≤21 mmHg).
  • MYOC mutations lead to intracellular protein retention, impaired aqueous outflow, and increased IOP.
  • OPTN and TBK1 mutations disrupt autophagy, potentially causing retinal ganglion cell damage.

Conclusions:

  • MYOC, OPTN, and TBK1 are key genes associated with Mendelian forms of glaucoma.
  • Abnormal MYOC protein handling and ER stress are implicated in MYOC-associated glaucoma.
  • Autophagy dysregulation is a potential mechanism for OPTN/TBK1-related normal tension glaucoma.
  • These genetic discoveries pave the way for novel, targeted glaucoma therapies.