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Related Concept Videos

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...
Chronic Pancreatitis II: Pathophysiology01:21

Chronic Pancreatitis II: Pathophysiology

Chronic pancreatitis is a progressive and irreversible inflammation of the pancreas, most often caused by long-term alcohol abuse, but it can also be related to ductal obstruction, smoking, or genetic factors.Chronic pancreatitis occurs when the pancreas is repeatedly exposed to harmful agents like alcohol, smoking, ductal obstruction, or genetic predisposition. These factors lead to the release of toxic metabolites and inflammatory cytokines, sustaining chronic inflammation in the pancreatic...
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...
Cholecystitis01:20

Cholecystitis

Cholecystitis is inflammation of the gallbladder, most commonly caused by obstruction of the cystic duct. This blockage prevents bile from draining, leading to gallbladder distension, inflammation, and potentially serious complications. This condition may present acutely or chronically and can happen with or without gallstones.EtiologyAbout 95% of cholecystitis cases are calculous, caused by gallstones blocking the cystic duct, leading to bile accumulation and inflammation of the gallbladder...
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...
Nephrotic Syndrome I : Introduction01:24

Nephrotic Syndrome I : Introduction

Nephrotic Syndrome is a chronic kidney disorder defined by clinical findings such as severe proteinuria, hypoalbuminemia, hyperlipidemia, and edema. These symptoms result from damage to the glomeruli, the kidney’s filtering units, increasing their permeability to proteins.Definition and Meaning:Proteinuria, defined as the loss of more than 3.5 grams of protein per day in adults, is a crucial feature of nephrotic syndrome. This condition is often accompanied by edema, the accumulation of fluid...

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Related Experiment Videos

Catecholoestrogens: possible role in systemic lupus erythematosus.

Wahid Ali Khan1, Moin Uddin, Mohd Wajid Ali Khan

  • 1Department of Clinical Biochemistry, College of Medicine and Medical Science, King Khalid University, Abha, KSA. wahidalikhan@rediffmail.com

Rheumatology (Oxford, England)
|August 5, 2009
PubMed
Summary

Catecholestrogens (CEs) may contribute to Systemic Lupus Erythematosus (SLE) development in women. CEs might cause DNA damage and alter immunogenicity, potentially inducing SLE autoantibodies.

Related Experiment Videos

Area of Science:

  • Immunology
  • Endocrinology
  • Molecular Biology

Background:

  • Systemic Lupus Erythematosus (SLE) disproportionately affects women, yet underlying mechanisms remain unclear.
  • Estrogen and its metabolites are implicated in SLE pathogenesis, but their precise role is elusive.
  • Preliminary evidence suggests catecholoestrogens (CEs) may play a role in SLE development.

Purpose of the Study:

  • To explore the potential role of catecholoestrogens (CEs) in the development of Systemic Lupus Erythematosus (SLE).
  • To investigate the proposed mechanism of CEs inducing DNA damage and autoantibody formation in SLE.

Main Methods:

  • The study discusses proposed mechanisms involving redox cycling of CEs.
  • Analysis of potential DNA damage induced by free radicals generated from CEs.
  • Evaluation of altered immunogenicity and autoantibody cross-reactivity with DNA.

Main Results:

  • CEs may undergo redox cycling, generating free radicals that can damage DNA.
  • This DNA damage could alter immunogenicity, potentially leading to SLE autoantibodies.
  • CEs might present unique neo-epitopes, contributing to SLE autoantibody induction.

Conclusions:

  • Catecholestrogens (CEs) present a potential mechanism in the induction of SLE autoantibodies.
  • CE-induced DNA damage and neo-epitope presentation are plausible factors in SLE pathogenesis.
  • The immunomodulatory role of estrogen in immune-related diseases, including SLE, warrants further investigation.