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

Acute Coronary Syndrome II: Pathophysiology and Clinical Manifestations01:19

Acute Coronary Syndrome II: Pathophysiology and Clinical Manifestations

369
The pathophysiology of Acute Coronary Syndrome [ACD] involves several key processes:The main underlying cause of ACD is atherosclerosis, a chronic inflammatory disease characterized by the buildup of lipid-laden plaques within the coronary arteries.As the atherosclerotic plaque grows in the coronary artery, it may become unstable due to the formation of a lipid-rich core and a thin fibrous cap. Inflammatory cells within the plaque, such as macrophages, secrete enzymes that degrade the...
369
Urinary Tract Calculi II: Pathophysiology and Clinical Manifestations01:26

Urinary Tract Calculi II: Pathophysiology and Clinical Manifestations

382
Renal calculi, commonly termed kidney stones, are crystalline solid masses that form in the kidneys but can occur at any point within the urinary system, encompassing the kidneys, ureters, bladder, and urethra.The pathophysiology of renal stones involves several key factors: supersaturation of the urine with stone-forming constituents, changes in urine pH, a decrease in urine volume, and the presence of substances that promote or inhibit stone formation.Supersaturation of Urine: This is the...
382
Esophageal Perforation-II: Clinical Manifestations and Management01:28

Esophageal Perforation-II: Clinical Manifestations and Management

518
Esophageal perforations manifest in various clinical forms, influenced by factors such as the perforation's cause and location (cervical, intrathoracic, or intra-abdominal), the extent of contamination, and potential injury to adjacent mediastinal structures. The timing between the perforation occurrence and treatment initiation also affects the clinical presentation.
Clinical Manifestations:
518
Barrett Esophagus-II: Clinical Manifestations and Management01:21

Barrett Esophagus-II: Clinical Manifestations and Management

824
Individuals with Barrett's esophagus are often asymptomatic, but they may experience symptoms commonly associated with GERD, such as heartburn and acid regurgitation. Additional symptoms can include difficulty swallowing, chest pain, unintentional weight loss, blood in the stool (which may appear black, tarry, or bloody), and episodes of vomiting.
To diagnose Barrett's esophagus, healthcare providers often recommend an endoscopy for those showing symptoms of acid reflux. The procedure...
824
Esophageal Varices-II: Clinical Features and Management01:28

Esophageal Varices-II: Clinical Features and Management

383
Esophageal varices often manifest as gastrointestinal bleeding episodes, presenting symptoms like hematemesis (vomiting of blood), hematochezia (passing fresh blood via the rectum), and melena (black, tarry stools). Other signs can include weight loss, anorexia, abdominal discomfort, jaundice, pruritus, altered mental status, and muscle cramps.
In the initial assessment, a thorough review of the patient's medical history is vital to identify risk factors such as liver disease, alcohol...
383
Gastritis III: Clinical Manifestations and Management01:23

Gastritis III: Clinical Manifestations and Management

1.2K
The clinical manifestations of gastritis can vary depending on the cause and type of gastritis, but some common symptoms may include the following.
Clinical manifestations of acute gastritis
The patient with acute gastritis may have a rapid onset of symptoms, such as epigastric pain or discomfort, dyspepsia, anorexia, hiccups, or nausea and vomiting, which can last from a few hours to a few days. Erosive or hemorrhagic gastritis may cause bleeding, which may manifest as blood in vomit or as...
1.2K

You might also read

Related Articles

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

Sort by
Same author

Real-world outcomes of pegcetacoplan treatment in C3 glomerulopathy and immune-complex membranoproliferative glomerulonephritis.

Kidney international·2026
Same author

Inhibition of Classical and Alternative Complement Pathway by Ravulizumab and Eculizumab.

Annals of clinical and translational neurology·2025
Same author

Profiling of proteases involved in SARS-CoV-2 pathogenesis in human saliva: Influence of age and gender.

Journal, genetic engineering & biotechnology·2025
Same author

Radiotherapy Upregulates the Expression of Membrane-Bound Negative Complement Regulator Proteins on Tumor Cells and Limits Complement-Mediated Tumor Cell Lysis.

Cancers·2025
Same author

External quality assurance program for diagnostic complement laboratories: evaluation of the results of the past seven years.

Frontiers in immunology·2024
Same author

Editorial: Contemporary challenges in immunologic testing in clinical and research laboratories.

Frontiers in immunology·2023

Related Experiment Video

Updated: Jan 20, 2026

Functional Complementation Analysis FCA: A Laboratory Exercise Designed and Implemented to Supplement the Teaching of Biochemical Pathways
09:27

Functional Complementation Analysis FCA: A Laboratory Exercise Designed and Implemented to Supplement the Teaching of Biochemical Pathways

Published on: June 24, 2016

18.2K

Complement deficiencies and dysregulation: Pathophysiological consequences, modern analysis, and clinical management.

Jutta Schröder-Braunstein1, Michael Kirschfink1

  • 1University of Heidelberg, Institute of Immunology, Im Neuenheimer Feld 305, 69120 Heidelberg, Germany.

Molecular Immunology
|August 18, 2019
PubMed
Summary

Complement deficiencies increase risks of infections and inflammatory disorders. Understanding these rare but severe conditions and their molecular basis is crucial for effective treatment.

Keywords:
Complement deficienciesComplement dysregulationDiagnosticsDiseaseReview

More Related Videos

The Murine Choline-Deficient, Ethionine-Supplemented CDE Diet Model of Chronic Liver Injury
07:27

The Murine Choline-Deficient, Ethionine-Supplemented CDE Diet Model of Chronic Liver Injury

Published on: October 21, 2017

12.3K
Identifying Dysregulated Genes Induced by Kaposi's Sarcoma-associated Herpesvirus KSHV
07:02

Identifying Dysregulated Genes Induced by Kaposi's Sarcoma-associated Herpesvirus KSHV

Published on: September 14, 2010

13.0K

Related Experiment Videos

Last Updated: Jan 20, 2026

Functional Complementation Analysis FCA: A Laboratory Exercise Designed and Implemented to Supplement the Teaching of Biochemical Pathways
09:27

Functional Complementation Analysis FCA: A Laboratory Exercise Designed and Implemented to Supplement the Teaching of Biochemical Pathways

Published on: June 24, 2016

18.2K
The Murine Choline-Deficient, Ethionine-Supplemented CDE Diet Model of Chronic Liver Injury
07:27

The Murine Choline-Deficient, Ethionine-Supplemented CDE Diet Model of Chronic Liver Injury

Published on: October 21, 2017

12.3K
Identifying Dysregulated Genes Induced by Kaposi's Sarcoma-associated Herpesvirus KSHV
07:02

Identifying Dysregulated Genes Induced by Kaposi's Sarcoma-associated Herpesvirus KSHV

Published on: September 14, 2010

13.0K

Area of Science:

  • Immunology
  • Genetics

Background:

  • Complement system defects heighten susceptibility to infections and inflammatory conditions.
  • These deficiencies, though rare, often manifest severely in childhood.
  • Autoantibodies can mimic inherited complement component deficiencies.

Purpose of the Study:

  • To provide an overview of clinical disorders linked to complement deficiencies and dysregulation.
  • To outline diagnostic strategies for molecular characterization of these conditions.
  • To emphasize the importance of molecular diagnosis for therapeutic decisions.

Main Methods:

  • Review of clinical disorders associated with complement deficiencies.
  • Description of diagnostic approaches for molecular characterization.
  • Analysis of the link between specific complement defects and associated diseases.

Main Results:

  • Defects in early classical pathway components correlate with autoimmune disorders.
  • Terminal pathway component deficiencies and properdin deficiency increase meningococcal infection risk.
  • Complement dysregulation is implicated in hereditary angioedema, atypical hemolytic uremic syndrome, C3 glomerulopathy, and age-related macular degeneration.

Conclusions:

  • Comprehensive molecular characterization is essential for managing complement-related disorders.
  • Identifying specific complement deficiencies guides therapeutic strategies.
  • Further research into complement pathways can improve patient outcomes.