Jove
Visualize
Contact Us

Related Concept Videos

Inflammatory Bowel Disease III: Crohn's Disease01:25

Inflammatory Bowel Disease III: Crohn's Disease

Crohn’s disease is a chronic, relapsing form of inflammatory bowel disease characterized by segmental, transmural inflammation that can affect any part of the gastrointestinal tract. Its pathogenesis arises from a combination of genetic susceptibility, environmental exposures, epithelial barrier dysfunction, and immune dysregulation. Together, these factors lead to an exaggerated immune response against components of the gut microbiome.Genetic and Environmental InfluencesMultiple genetic...
Inflammatory Bowel Disease IV: Pharmacological Management01:29

Inflammatory Bowel Disease IV: Pharmacological Management

Upon diagnosis, managing Inflammatory Bowel Disease (IBD) involves addressing several crucial aspects. The primary goals include resting the bowel, correcting malnutrition, and providing symptomatic relief. Resting the bowel may consist of medications to reduce inflammation and promote healing. Correcting malnutrition is essential, often requiring dietary adjustments and nutritional supplements. Symptomatic relief aims to ease pain, diarrhea, and other discomforts in IBD.
Pharmacologic...
Nephrotic Syndrome II : Assessment and Medical Management01:26

Nephrotic Syndrome II : Assessment and Medical Management

IntroductionNephrotic syndrome is a kidney disorder marked by excessive protein loss in the urine, leading to various systemic complications. This condition often results from damage to the glomeruli—the kidney's filtering units—causing proteinuria, low blood protein levels, and fluid retention. Understanding the assessment, diagnosis, and management of nephrotic syndrome is essential for effective treatment and prevention of further kidney damage.AssessmentPatient History: Document any history...
Gastritis-II: Pathophysiology01:17

Gastritis-II: Pathophysiology

Gastritis is marked by disruption of the mucosal barrier that usually protects the stomach tissue from digestive juices and manifests in acute and chronic forms.
In acute gastritis, the gastric mucosa becomes swollen and red and undergoes superficial erosion. Superficial ulceration may lead to bleeding.
In chronic gastritis, persistent or repeated insults lead to chronic inflammatory changes and, eventually, thinning or atrophy of the gastric tissue.
Gastritis can stem from various causes, each...
Gastritis II: Pathophysiology01:26

Gastritis II: Pathophysiology

The pathophysiology of gastritis begins with the colonization of the stomach lining by Helicobacter pylori (H. pylori). This bacterium spreads mainly via the oral-oral route through saliva or shared utensils, and can also be transmitted in overcrowded or unhygienic environments through contaminated water, despite its brief survival outside the body.ColonizationOnce ingested, H. pylori enters the stomach and begins colonization by navigating through the mucus layer lining the stomach wall. It...
Inflammatory Bowel Disease III: Diagnostic Studies and Management I-Nutritional Therapy01:30

Inflammatory Bowel Disease III: Diagnostic Studies and Management I-Nutritional Therapy

Various diagnostic tests are employed in the diagnostic process for Inflammatory Bowel Disease (IBD), particularly to differentiate between Crohn's disease and ulcerative colitis.
Diagnostic studies
A colonoscopy is the definitive screening test, distinguishing ulcerative colitis from other colon diseases with similar symptoms. During a colonoscopy test, inflamed mucosa with exudate ulcerations can be observed, and biopsies are taken to determine the histologic characteristics of the colonic...

You might also read

Related Articles

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

Sort by
Same author

Infliximab in refractory spondyloarthropathies: a multicentre 38 week open study.

Annals of the rheumatic diseases·2003
See all related articles
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 Experiment Videos

[Psoriatic synovitis: pathogenic and therapeutic implications].

J D Cañete-Crespillo1

  • 1Unidad de Artritis. Servicio de Reumatología. Hospital Clínic de Barcelona. España.

Reumatologia Clinica
|July 29, 2011
PubMed
Summary
This summary is machine-generated.

Psoriatic arthritis (PsA) is a complex autoimmune disease. Research highlights differences in synovial tissue between PsA and rheumatoid arthritis, suggesting targeted therapies for PsA.

Related Experiment Videos

Area of Science:

  • Rheumatology
  • Immunology
  • Dermatology

Context:

  • Psoriatic arthritis (PsA) is a chronic inflammatory autoimmune disease affecting joints and skin.
  • Clinical heterogeneity of PsA complicates research and clinical trials.
  • Biologic agents have increased interest in PsA pathogenesis and classification.

Purpose:

  • To review recent articles on PsA pathogenesis.
  • To focus on synovial angiogenesis as a therapeutic target.
  • To discuss synovial expression of macrophages and p53 in PsA and rheumatoid arthritis (RA).

Summary:

  • PsA pathogenesis is complex, with potential therapeutic targets in synovial angiogenesis.
  • Synovial expression of macrophages and p53 protein is linked to joint damage in PsA and RA.
  • The polyarticular variant of PsA may share features with RA or spondyloarthropathies (SpA), but distinct immunohistochemical profiles exist.

Impact:

  • Understanding differences in PsA pathogenesis could lead to specific therapies.
  • Identifying unique cellular and molecular pathways in PsA may improve treatment strategies.
  • This review aids in classifying PsA and understanding its underlying mechanisms.