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

Spinal Cord Injury ll: Pathophysiology01:14

Spinal Cord Injury ll: Pathophysiology

Spinal cord injury progresses through two interconnected phases: primary injury and secondary injury.Primary InjuryPrimary injury happens at the moment of trauma and involves immediate mechanical damage to the spinal cord.Compression happens when broken vertebrae, herniated discs, or accumulating blood (such as a hematoma) press directly against the spinal cord, distorting its normal shape and function. In cases of contusion, the cord is bruised by a blunt force (like penetrating injuries or...
Secondary Spinal Cord Injury llI: Pathophysiology01:25

Secondary Spinal Cord Injury llI: Pathophysiology

Early Ischemia and Ionic ImbalanceWithin minutes of spinal cord injury, a secondary cascade begins, progressing over hours to weeks. Vascular damage reduces blood flow, causing ischemia and mitochondrial dysfunction. ATP depletion leads to ion pump failure, membrane depolarization, sodium influx, potassium efflux, and water accumulation, resulting in cellular swelling. Increased intracellular calcium further disrupts mitochondria and accelerates cellular injury.Excitotoxicity and Neuronal...
Power System Three-Phase Short Circuits01:21

Power System Three-Phase Short Circuits

Determining the subtransient fault current in a power system involves representing transformers by their leakage reactances, transmission lines by their equivalent series reactances, and synchronous machines as constant voltage sources behind their subtransient reactances. In this analysis, certain elements are excluded, such as winding resistances, series resistances, shunt admittances, delta-Y phase shifts, armature resistance, saturation, saliency, non-rotating impedance loads, and small...
Increased Intracranial Pressure ll: Pathophysiology01:29

Increased Intracranial Pressure ll: Pathophysiology

Increased intracranial pressure (ICP) refers to a potentially life-threatening rise in pressure inside the skull. This usually happens when there is a major change in the volume of brain tissue, blood, or cerebrospinal fluid (CSF) — the three components inside the skull. According to the Monro-Kellie doctrine, if the volume of one component increases, the volumes of the other components must decrease to maintain normal pressure. If this does not happen, ICP rises.The process often begins with...
Electrophysiology of Normal Cardiac Rhythm01:19

Electrophysiology of Normal Cardiac Rhythm

The normal cardiac rhythm is a synchronized electrical activity that facilitates the regular and coordinated contraction of the heart muscle. This process is essential for efficient blood circulation throughout the body. The fundamental elements involved in establishing and maintaining this rhythm include the unique electrical properties of cardiac muscle cells, the sinoatrial (SA) node's pacemaker function, the specialized conducting system, and the ionic mechanisms underlying each phase of...
Pathophysiology of Cardiac Performance01:29

Pathophysiology of Cardiac Performance

Typical heart performance is influenced by heart rate, rhythm, myocardial contraction, and metabolism or blood flow. The cardiac muscle exhibits distinct electrophysiological features, including pacemaker activity and calcium channel control, which play a vital role in the heart's response to various drugs. The autonomic nervous system, comprising the sympathetic and parasympathetic branches, regulates heart rate. Sympathetic activation increases heart rate, while parasympathetic activation...

You might also read

Related Articles

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

Sort by
Same author

Severe psychotic disorder and agranulocytosis--a therapeutic dilemma.

Pharmacopsychiatry·2009
Same author

Prospective evaluation of PF4/heparin immunoassays for the diagnosis of heparin-induced thrombocytopenia.

Journal of thrombosis and haemostasis : JTH·2009
Same author

Screening of multiparous women to avoid transfusion-related acute lung injury: a single centre experience.

Transfusion medicine (Oxford, England)·2009
Same author

[Diagnosis of idiopathic thrombocytopenic purpura].

Hamostaseologie·2008
Same author

Heparin-independent activation of platelets by heparin-induced thrombocytopenia antibodies: a common occurrence.

Journal of thrombosis and haemostasis : JTH·2007
Same author

Platelets in atherothrombosis: lessons from mouse models.

Journal of thrombosis and haemostasis : JTH·2005

Related Experiment Video

Updated: Jul 13, 2026

Technique and Considerations in the Use of 4x1 Ring High-definition Transcranial Direct Current Stimulation (HD-tDCS)
15:05

Technique and Considerations in the Use of 4x1 Ring High-definition Transcranial Direct Current Stimulation (HD-tDCS)

Published on: July 14, 2013

Pathophysiology of TRALI: current concepts.

U J H Sachs1

  • 1Institute for Clinical Immunology and Transfusion Medicine, Justus Liebig University, Langhansstr. 7, 35392 Giessen, Germany. ulrich.sachs@med.uni-giessen.de

Intensive Care Medicine
|November 2, 2007
PubMed
Summary

Transfusion-related acute lung injury (TRALI) is a fatal complication of blood transfusion. Current evidence supports immediate preventive measures for immune TRALI, while non-immune TRALI requires further research.

Area of Science:

  • Hematology
  • Immunology
  • Critical Care Medicine

Background:

  • Transfusion-related acute lung injury (TRALI) is a leading cause of transfusion fatalities in the US and UK.
  • TRALI shares clinical definitions with acute respiratory distress syndrome (ARDS) but is directly linked to blood transfusions.
  • Two primary mechanisms, leuko-agglutination and a two-event lipid model, are proposed for TRALI pathogenesis.

Purpose of the Study:

  • To review the pathophysiology of TRALI, including immune and non-immune mechanisms.
  • To examine unresolved questions regarding TRALI, such as the role of HLA class-II antibodies and endothelial participation.
  • To discuss preventive strategies for both immune and non-immune TRALI.

Main Methods:

  • Literature review and synthesis of existing clinical and experimental data on TRALI.

More Related Videos

Home-Based Transcranial Direct Current Stimulation Device Development: An Updated Protocol Used at Home in Healthy Subjects and Fibromyalgia Patients
11:26

Home-Based Transcranial Direct Current Stimulation Device Development: An Updated Protocol Used at Home in Healthy Subjects and Fibromyalgia Patients

Published on: July 14, 2018

Related Experiment Videos

Last Updated: Jul 13, 2026

Technique and Considerations in the Use of 4x1 Ring High-definition Transcranial Direct Current Stimulation (HD-tDCS)
15:05

Technique and Considerations in the Use of 4x1 Ring High-definition Transcranial Direct Current Stimulation (HD-tDCS)

Published on: July 14, 2013

Home-Based Transcranial Direct Current Stimulation Device Development: An Updated Protocol Used at Home in Healthy Subjects and Fibromyalgia Patients
11:26

Home-Based Transcranial Direct Current Stimulation Device Development: An Updated Protocol Used at Home in Healthy Subjects and Fibromyalgia Patients

Published on: July 14, 2018

  • Discussion of proposed pathophysiological pathways, including granulocyte activation.
  • Analysis of the clinical relevance of different TRALI mechanisms.
  • Main Results:

    • Immune TRALI involves leukocyte antibodies, while non-immune TRALI may involve lipids accumulating during storage.
    • Granulocyte activation is an emerging common pathway in TRALI.
    • Further data are needed for non-immune TRALI, but preventive measures for immune TRALI are recommended.

    Conclusions:

    • Immediate preventive measures against transfusing blood products with leukocyte antibodies are crucial for immune TRALI.
    • Further clinical and experimental research is necessary to establish recommendations for non-immune TRALI.
    • Understanding TRALI pathophysiology is essential for improving transfusion safety and patient outcomes.