Search research articles

ABOUT JoVE

Overview Leadership Blog JoVE Help Center

AUTHORS

Publishing Process Editorial Board Scope & Policies Peer Review FAQ Submit

LIBRARIANS

Testimonials Subscriptions Access Resources Library Advisory Board FAQ

RESEARCH

JoVE Journal Methods Collections JoVE Encyclopedia of Experiments Archive

EDUCATION

JoVE Core JoVE Business JoVE Science Education JoVE Lab Manual Faculty Resource Center Faculty Site

Terms & Conditions of Use

Related Concept Videos

Biological Effects of Radiation

Biological Effects of Radiation

All radioactive nuclides emit high-energy particles or electromagnetic waves. When this radiation encounters living cells, it can cause heating, break chemical bonds, or ionize molecules. The most serious biological damage results when these radioactive emissions fragment or ionize molecules. For example, α and β particles emitted from nuclear decay reactions possess much higher energies than ordinary chemical bond energies. When these particles strike and penetrate matter, they...

You might also read

Related Articles

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

Sort by

Same author

4D-aware stereo matching via implicit spectral reconstruction with multi-modal training and RGB-only deployment.

Optics express·2026

Same author

Replication-stress-induced chromatin loops protect fork stability.

Nature·2026

Same author

Weakly Textured Objects Pose Estimation: A Comprehensive Review.

Sensors (Basel, Switzerland)·2026

Same author

CDCA7 targets LSH to DNA maintenance methylation in S phase and transcription regulation in interphase via two distinct DNA-binding modes.

Nucleic acids research·2026

Same author

Functional orthopedic treatment for mandibular asymmetry in a giant panda with amputation.

The Angle orthodontist·2026

Same author

Rbm25 governs embryonic stem cell identity and fate through transcriptional regulation of pluripotency and epigenetic programs.

Stem cell reports·2025

Search research articles

Related Experiment Video

Updated: Apr 9, 2026

Neutrophil Isolation and Analysis to Determine their Role in Lymphoma Cell Sensitivity to Therapeutic Agents

Neutrophil Isolation and Analysis to Determine their Role in Lymphoma Cell Sensitivity to Therapeutic Agents

Published on: March 25, 2016

Galectin-9^high Neutrophils Exacerbate Radiation-Induced Frailty.

Zhuo Cheng¹, Le Ma¹, Yan Chen¹

¹Institute of Rocket Force Medicine, State Key Laboratory of Trauma and Chemical Poisoning, Army Medical University, Chongqing, China.

|April 7, 2026

Summary

Radiation injury causes frailty via hyperactive GAL-9 high neutrophils. These cells disrupt organs and bone marrow, exacerbating patient frailty and impacting quality of life.

More Related Videos

Establishment of a Robust and Reproducible Model of Radiation-Induced Skin and Muscle Fibrosis

Establishment of a Robust and Reproducible Model of Radiation-Induced Skin and Muscle Fibrosis

Published on: August 31, 2022

Author Spotlight: Assessing Surgical Frailty with Point-of-Care Ultrasound of Quadriceps Muscles

Author Spotlight: Assessing Surgical Frailty with Point-of-Care Ultrasound of Quadriceps Muscles

Published on: July 26, 2024

Related Experiment Videos

Last Updated: Apr 9, 2026

Neutrophil Isolation and Analysis to Determine their Role in Lymphoma Cell Sensitivity to Therapeutic Agents

Neutrophil Isolation and Analysis to Determine their Role in Lymphoma Cell Sensitivity to Therapeutic Agents

Published on: March 25, 2016

Establishment of a Robust and Reproducible Model of Radiation-Induced Skin and Muscle Fibrosis

Establishment of a Robust and Reproducible Model of Radiation-Induced Skin and Muscle Fibrosis

Published on: August 31, 2022

Author Spotlight: Assessing Surgical Frailty with Point-of-Care Ultrasound of Quadriceps Muscles

Author Spotlight: Assessing Surgical Frailty with Point-of-Care Ultrasound of Quadriceps Muscles

Published on: July 26, 2024

Area of Science:

Radiation biology
Immunology
Hematology

Background:

Local radiation injury can cause frailty, significantly impacting patient quality of life and incurring substantial medical costs.
The precise mechanisms driving radiation-induced frailty remain largely unknown, necessitating further investigation into cellular and molecular pathways.

Purpose of the Study:

To elucidate the underlying mechanisms of radiation injury-induced frailty.
To identify key cellular players and molecular pathways involved in the exacerbation of frailty following radiation exposure.

Main Methods:

Identification and characterization of a unique neutrophil population (GAL-9 high) with specific functional attributes.
Investigation of neutrophil infiltration, bone marrow microenvironment disruption, and macrophage clearance resistance.
Analysis of the role of GAL-9 protein in neutrophil hyperactivity and the JAK1/2-STAT1 pathway activation in splenic GMP cells via eccDNA.

Main Results:

A novel population of hyperactive GAL-9 high neutrophils was identified, exhibiting elevated reactive oxygen species (ROS), neutrophil extracellular traps (NETs), and interferon-gamma (IFN-γ), along with a prolonged lifespan.
These GAL-9 high neutrophils infiltrate multiple organs, causing injury, disrupting the bone marrow microenvironment, promoting myeloid-biased differentiation, and evading macrophage clearance, thereby worsening frailty.
Extrachromosomal circular DNA (eccDNA) shedding post-radiation activates the JAK1/2-STAT1 pathway in splenic GMP cells, representing a potential source of these GAL-9 high neutrophils.

Conclusions:

Hyperactive GAL-9 high neutrophils are a critical factor in exacerbating frailty after local radiation injury.
The identified 'skin-spleen-bone marrow-multiple organs' axis highlights a novel pathway through which radiation-induced frailty develops.
Targeting GAL-9 or the JAK1/2-STAT1 pathway may offer therapeutic strategies to mitigate radiation-induced frailty.