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

Directly Acting Muscle Relaxants: Dantrolene and Botulinum Toxin01:26

Directly Acting Muscle Relaxants: Dantrolene and Botulinum Toxin

1.3K
Directly acting muscle relaxants like dantrolene and botulinum toxin (BoNT) have distinct mechanisms and applications. Dantrolene, a hydantoin derivative, acts on the ryanodine receptor (RYR1) in skeletal muscle cells. RYR1 are calcium channels present at the sarcoplasmic reticulum membrane. In response to excitation, they release calcium ions from the sarcoplasmic reticulum to the cytosol. Calcium promotes actin-myosin-mediated contraction of muscles.
The binding of dantrolene to the RYR1...
1.3K
Prevention of Further Absorption of Poison01:14

Prevention of Further Absorption of Poison

1.3K
In cases of acute poisoning, the primary objective is to prevent further absorption of the toxic substance into the body. Immediate interventions using various decontamination techniques targeting the gastrointestinal (GI) tract can achieve this. Decontamination is crucial to prevent poison from entering the systemic circulation, which involves washing affected areas with water and mild soap and removing contaminated clothing. Once external decontamination is done, attention must be turned to...
1.3K
Pharmaceutical Poisoning: Treatment Strategies01:26

Pharmaceutical Poisoning: Treatment Strategies

52
Treatment strategies for poisoning are a critical aspect of emergency medicine, focusing on preventing the absorption of toxins and enhancing their elimination. When a poisoning incident occurs, the first response is to halt exposure and decontaminate the patient, particularly through gastrointestinal (GI) methods if the poison was ingested.Gastrointestinal Decontamination Techniques:Activated charcoal is the cornerstone of GI decontamination. It works through adsorption, binding the toxin to...
52
Antidotes01:17

Antidotes

1.2K
Antidotes are medicinal substances used to counteract the harmful effects of toxins or drugs in the body. They function in various ways, each uniquely designed to combat specific toxic compounds.
Specific antidotes operate by inhibiting the enzymes that control biochemical pathways, reducing the production of harmful metabolites.
An example of an antidote is atropine, which counteracts the detrimental effects of cholinesterase inhibitors. It achieves this by deactivating muscarinic receptors,...
1.2K
Anticholinesterase Agents: Poisoning and Treatment01:26

Anticholinesterase Agents: Poisoning and Treatment

1.8K
Anticholinesterases, also known as cholinesterase inhibitors, work by blocking the breakdown of acetylcholine, leading to its accumulation in the synaptic cleft. This accumulation indirectly enhances both muscarinic and nicotinic actions. These agents are classified as reversible or irreversible based on their mechanism of action.     
Irreversible agents form a strong bond with the cholinesterase enzyme, making it inactive. The breakdown of the phosphorylated enzyme is...
1.8K
Gene Regulation in Microbial Communities: Quorum Sensing01:28

Gene Regulation in Microbial Communities: Quorum Sensing

752
Quorum sensing is a mechanism of bacterial communication that enables coordinated gene expression in response to changes in population density. This facilitates collective behaviors that enhance survival, resource acquisition, and ecological adaptation. This process relies on small signaling molecules called autoinducers that accumulate as bacterial populations grow. When a critical threshold concentration of autoinducers is reached, bacterial cells collectively modify gene expression,...
752

You might also read

Related Articles

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

Sort by
Same author

SARS-CoV-2 (MA10) Infection Aggravates Cerebrovascular Pathology in Endothelial Nitric Oxide Synthase-Deficient Mice.

Viruses·2025
Same author

Imaging Interstitial Fluids and Extracellular Matrix in Cerebrovascular Disorders: Current Perspectives and Clinical Applications.

Neuroimaging clinics of North America·2025
Same author

Neurological sequelae of long COVID: a comprehensive review of diagnostic imaging, underlying mechanisms, and potential therapeutics.

Frontiers in neurology·2025
Same author

A patient-centric chest pain management approach utilizing a high sensitivity Troponin-I assay.

Heliyon·2024
Same author

Ultra-low-level measurements of airborne fission products from the Fukushima Daiichi reactor accident using high volume collection systems at Savannah River National Laboratory.

Journal of environmental radioactivity·2022
Same author

Infection of Immunocompetent Conventional Mice with Shiga Toxin-Producing E. coli: The DSS + STEC Model.

Methods in molecular biology (Clifton, N.J.)·2021
Same journal

Chemical, Biological, and Ecological Evidence for Aerobic Deoxynivalenol Detoxification in Agronomic Soil-Derived Bacterial Communities.

Toxins·2026
Same journal

Botulinum Toxin Treatment for Uncommon Phenotypes of Laryngeal Adductor Breathing Dystonia.

Toxins·2026
Same journal

Enhancing Neuronal Networks with <i>Rhinella schneideri</i> Skin Secretion Molecules: Implications for Neurodegenerative Disorders.

Toxins·2026
Same journal

Dangerous Measures: A Case Report and Review of Motoro Ray Envenomation.

Toxins·2026
Same journal

The Impact of OnabotulinumtoxinA on Oral Pain Medication Prescription Fills and Low-Value Care in Patients with Cervical Dystonia in the United States: A Retrospective Claims Analysis.

Toxins·2026
Same journal

Broad-Spectrum Antiviral and Antibacterial Activity of the Scorpion Venom Peptide HP1090.

Toxins·2026
See all related articles

Related Experiment Video

Updated: Feb 22, 2026

A High-throughput-compatible FRET-based Platform for Identification and Characterization of Botulinum Neurotoxin Light Chain Modulators
10:30

A High-throughput-compatible FRET-based Platform for Identification and Characterization of Botulinum Neurotoxin Light Chain Modulators

Published on: December 27, 2013

5.8K

Shiga Toxin Therapeutics: Beyond Neutralization.

Gregory Hall1, Shinichiro Kurosawa2, Deborah J Stearns-Kurosawa3

  • 1Department of Pathology and Laboratory Medicine, Boston University School of Medicine, Boston, MA 02118, USA. grhall@bu.edu.

Toxins
|September 20, 2017
PubMed
Summary
This summary is machine-generated.

Shiga toxins from E. coli cause hemolytic uremic syndrome (HUS), a severe condition in children. Targeting cellular responses like the unfolded protein response (UPR) may offer new therapeutic strategies for HUS.

Keywords:
STECSTX1STX2Shiga toxinShiga toxin-producing E. coliShiga-like toxinshemolytic uremic syndromeribotoxic stress responseribotoxinunfolded protein response

More Related Videos

A High Content Imaging Assay for Identification of Botulinum Neurotoxin Inhibitors
14:10

A High Content Imaging Assay for Identification of Botulinum Neurotoxin Inhibitors

Published on: November 14, 2014

9.0K
Detection of Toxin Translocation into the Host Cytosol by Surface Plasmon Resonance
10:41

Detection of Toxin Translocation into the Host Cytosol by Surface Plasmon Resonance

Published on: January 3, 2012

13.8K

Related Experiment Videos

Last Updated: Feb 22, 2026

A High-throughput-compatible FRET-based Platform for Identification and Characterization of Botulinum Neurotoxin Light Chain Modulators
10:30

A High-throughput-compatible FRET-based Platform for Identification and Characterization of Botulinum Neurotoxin Light Chain Modulators

Published on: December 27, 2013

5.8K
A High Content Imaging Assay for Identification of Botulinum Neurotoxin Inhibitors
14:10

A High Content Imaging Assay for Identification of Botulinum Neurotoxin Inhibitors

Published on: November 14, 2014

9.0K
Detection of Toxin Translocation into the Host Cytosol by Surface Plasmon Resonance
10:41

Detection of Toxin Translocation into the Host Cytosol by Surface Plasmon Resonance

Published on: January 3, 2012

13.8K

Area of Science:

  • Microbiology
  • Toxicology
  • Pediatric Nephrology

Background:

  • Shiga toxins produced by enterohemorrhagic Escherichia coli (STEC) are the primary cause of hemolytic uremic syndrome (HUS).
  • HUS is a significant cause of acute kidney injury and renal failure in children, with substantial mortality and morbidity rates.
  • Current therapeutic options for STEC-induced HUS are limited, despite extensive research into Shiga toxin mechanisms.

Purpose of the Study:

  • To review potential therapeutic strategies for HUS by targeting downstream cellular effects of Shiga toxins.
  • To explore the role of the unfolded protein response (UPR) and ribotoxic stress response (RSR) in HUS pathogenesis.
  • To identify therapeutic avenues that leverage existing drug development for other diseases with similar cellular pathway involvement.

Main Methods:

  • Review of existing literature on Shiga toxin toxicity, HUS pathogenesis, and cellular stress responses.
  • Analysis of the unfolded protein response (UPR) and ribotoxic stress response (RSR) pathways in the context of Shiga toxin-induced cellular damage.
  • Evaluation of the potential for therapeutic targeting of UPR and RSR pathways.

Main Results:

  • Shiga toxins induce cellular damage through mechanisms involving the UPR and RSR.
  • These cellular responses are implicated in the pathogenesis of HUS.
  • Targeting UPR and RSR pathways presents a promising therapeutic strategy for HUS.

Conclusions:

  • Therapeutic targeting of the UPR and RSR offers a viable approach to developing treatments for STEC-induced HUS.
  • The relevance of UPR and RSR to other prevalent diseases can facilitate drug development for HUS.
  • Developing drugs for these cellular pathways could improve outcomes for patients with STEC-HUS and potentially other related conditions.