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

Diabetic Foot Ulcer01:31

Diabetic Foot Ulcer

Definition A diabetic foot ulcer (DFU) is a chronic, non-healing wound that develops in individuals with diabetes. It typically occurs on pressure-bearing areas such as the heel, metatarsal heads, or hallux, and carries a high risk of infection and amputation.Pathophysiology • The development of DFUs can be explained by four interconnected mechanisms: neuropathy, ischemia, infection, and impaired wound healing. • Neuropathy is the most common factor. Sensory neuropathy reduces pain perception,...
Inflammatory Response II: Inflammatory Exudate and Tissue Repair01:24

Inflammatory Response II: Inflammatory Exudate and Tissue Repair

The immune system's inflammatory response destroys the invading pathogen, permitting the tissue to heal. The changes during the cellular and vascular stages allow exudate formation at the site of inflammation. The inflammatory exudate released from the wound has high protein content and a specific gravity above 1.020.
The typical wound exudate is odorless, transparent, straw-colored, thin, and watery. Exudate, however, can differ depending on the state of wound healing. Likewise, the exudate's...
Acute Kidney Injury II: Pathophysiology01:29

Acute Kidney Injury II: Pathophysiology

Acute kidney injury (AKI) causes are categorized into three primary categories based on the location of the injury: prerenal, intrarenal (or intrinsic), and postrenal causes. This classification guides clinical management and illustrates how different pathways can impair kidney function.Etiology and Pathophysiology of Acute Kidney Injury1. Prerenal causesEtiology: Prerenal Acute Kidney Injury, the most common type, occurs when reduced blood flow to the kidneys decreases filtration capacity...
Acute Kidney Injury IV: Diagnostic Studies and Prevention01:30

Acute Kidney Injury IV: Diagnostic Studies and Prevention

Accurate diagnosis and effective prevention are critical in managing Acute Kidney Injury (AKI), which is linked to high mortality rates ranging from 10% to 80%. Timely recognition of at-risk patients and careful monitoring can significantly reduce the likelihood of kidney damage.Diagnostic Assessments:The diagnostic process starts with a comprehensive medical history to identify prerenal, intrarenal, and postrenal causes.Prerenal causes, such as dehydration, hypotension, or blood loss, should...
Peptic Ulcer01:27

Peptic Ulcer

Peptic ulcers are erosive lesions of the gastric or duodenal lining, most commonly caused by Helicobacter pylori infection. This Gram-negative, helical bacterium has adapted to survive the stomach’s acidic environment by producing urease, which converts urea into ammonia and carbon dioxide. The ammonia neutralizes gastric acid in the bacterium’s immediate environment, allowing colonization of the gastric mucosa. H. pylori attaches to mucus-secreting epithelial cells, penetrates the mucus...
Acute Kidney Injury III: Clinical Manifestations01:29

Acute Kidney Injury III: Clinical Manifestations

Acute Kidney Injury (AKI) progresses through distinct clinical phases: the oliguric, diuretic, and recovery phases, each marked by unique manifestations and challenges.Oliguric Phase:The oliguric phase is the initial stage of AKI, typically lasting 10 to 14 days. This phase is marked by a significant reduction in urine output, usually less than 400 mL per day, indicating decreased kidney function. Fluid retention is a prominent feature, leading to symptoms such as edema, hypertension, and...

You might also read

Related Articles

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

Sort by
Same author

Cognitive Impairment in People With Diabetes-Related Foot Ulcers: A Multicentre, Case-Control, Observational Study.

International wound journal·2026
Same author

An Association Between Haemochromatosis Genotypes and Venous Leg Ulcers in Australian Individuals.

Wound repair and regeneration : official publication of the Wound Healing Society [and] the European Tissue Repair Society·2026
Same author

Disease-Specific Distress in Adults With Venous Leg Ulcers: An Integrative Review.

Journal of wound, ostomy, and continence nursing : official publication of The Wound, Ostomy and Continence Nurses Society·2025
Same author

Evaluation of the Construct Validity of a Risk Assessment Instrument for Venous Leg Ulcer Recurrence.

Journal of wound, ostomy, and continence nursing : official publication of The Wound, Ostomy and Continence Nurses Society·2025
Same author

Wound education opportunities for rural and regional health care sectors of Australia. A scoping review.

Journal of tissue viability·2025
Same author

Measurement and Sequelae of Neonatal Skin Injuries: A Prospective Diagnostic/Feasibility Study.

International wound journal·2025

Related Experiment Video

Updated: May 28, 2026

Collecting And Measuring Wound Exudate Biochemical Mediators In Surgical Wounds
04:58

Collecting And Measuring Wound Exudate Biochemical Mediators In Surgical Wounds

Published on: October 20, 2012

Elevated uric acid correlates with wound severity.

Melissa L Fernandez1, Zee Upton, Helen Edwards

  • 1Tissue Repair and Regeneration Program, Cells and Tissues Domain, Institute of Health and Biomedical Innovation, Queensland University of Technology, Kelvin Grove, QLD, Australia. ml.fernandez@qut.edu.au

International Wound Journal
|October 7, 2011
PubMed
Summary
This summary is machine-generated.

Uric acid (UA) is elevated in chronic venous leg ulcers, correlating with wound severity. Xanthine oxidase activity suggests it prolongs inflammation, impacting chronic wound healing.

Related Experiment Videos

Last Updated: May 28, 2026

Collecting And Measuring Wound Exudate Biochemical Mediators In Surgical Wounds
04:58

Collecting And Measuring Wound Exudate Biochemical Mediators In Surgical Wounds

Published on: October 20, 2012

Area of Science:

  • Biomedical research
  • Wound healing science
  • Biochemistry of chronic wounds

Background:

  • Chronic venous leg ulcers are a significant health concern.
  • Understanding chronic wound formation is crucial for developing new treatments.
  • Current research on chronic wound pathophysiology is limited.

Purpose of the Study:

  • To investigate the role of uric acid (UA) in chronic venous leg ulcers.
  • To explore the relationship between UA levels, wound chronicity, and severity.
  • To determine the activity of xanthine oxidase in chronic wound fluid.

Main Methods:

  • Analysis of wound fluid (WF) from chronic venous leg ulcers.
  • Quantification of uric acid (UA) and its precursors, like adenosine.
  • Assay for xanthine oxidase activity in WF.

Main Results:

  • Elevated uric acid (UA) levels were observed in chronic venous leg ulcer wound fluid (WF).
  • Higher UA concentrations correlated with increased wound chronicity.
  • Depletion of UA precursors (e.g., adenosine) corresponded with greater wound severity.
  • Xanthine oxidase was found to be active in chronic WF.

Conclusions:

  • Uric acid (UA) is a potential biomarker for chronic venous leg ulcer chronicity.
  • Xanthine oxidase activity in chronic wounds may prolong inflammation.
  • This suggests xanthine oxidase plays a critical role in chronic wound formation.