Investigating head responses during hockey-related blunt impacts and hence understanding how to mitigate brain injury risk from such impacts still needs more exploration. This study used the recently developed hockey helmet testing methodology, known as the Hockey Summation of Tests for the Analysis of Risk (Hockey STAR), to collect 672 laboratory helmeted impacts. Brain strains were then calculated from the according 672 simulations using the detailed Global Human Body Models Consortium (GHBMC) finite element head model. Experimentally measured head kinematics and brain strains were used to calculate head/brain injury metrics including peak linear acceleration, peak rotational acceleration, peak rotational velocity, Gadd Severity Index (GSI), Head Injury Criteria (HIC), Generalized Acceleration Model for Brain Injury Threshold (GAMBIT), Brain Injury Criteria (BrIC), Universal Brain Injury Criterion (UBrIC), Diffuse Axonal Multi-Axis General Equation (DAMAGE), average maximum principal strain (MPS) and cumulative strain damage measure (CSDM). Correlation analysis of kinematics-based and strain-based metrics highlighted the importance of rotational velocity. Injury metrics that use rotational velocity correlated highly to average MPS and CSDM with UBrIC yielding the strongest correlation. In summary, a comprehensive analysis for kinematics-based and strain-based injury metrics was conducted through a hybrid experimental (672 impacts) and computational (672 simulations) approach. The results can provide references for adopting brain injury metrics when using the Hockey STAR approach and guide ice hockey helmet designs that help reduce brain injury risks.
Download full-text PDF |
Source |
---|---|
http://dx.doi.org/10.1007/s10439-021-02855-3 | DOI Listing |
Alzheimers Dement
December 2024
Case Western Reserve University, Cleveland, OH, USA.
Background: Traumatic Brain Injury (TBI) is one of the most common nonheritable causes of Alzheimer's disease (AD). However, there is lack of effective treatment for both AD and TBI. We posit that network-based integration of multi-omics and endophenotype disease module coupled with large real-world patient data analysis of electronic health records (EHR) can help identify repurposable drug candidates for the treatment of TBI and AD.
View Article and Find Full Text PDFAlzheimers Dement
December 2024
NYU Grossman School of Medicine, New York, NY, USA; NYU, New York City, NY, USA.
Background: Astrocytes, a major glial cell in the central nervous system (CNS), can become reactive in response to inflammation or injury, and release toxic factors that kill specific subtypes of neurons. Over the past several decades, many groups report that reactive astrocytes are present in the brains of patients with Alzheimer's disease, as well as several other neurodegenerative diseases. In addition, reactive astrocyte sub-types most associated with these diseases are now reported to be present during CNS cancers of several types.
View Article and Find Full Text PDFAlzheimers Dement
December 2024
Xuanwu Hospital of Capital Medical University, Beijing, Beijing, China.
Background: Cerebral small vessel disease (CSVD) is one of the most common nervous system diseases. Hypertension and neuroinflammation are considered important risk factors for the development of CSVD and white matter (WM) lesions.
Method: We used the spontaneously hypertensive rat (SHR) as a model of early-onset CSVD and administered epimedium flavonoids (EF) for three months.
Background: Neuroinflammation is a critical factor of Alzheimer's Disease (AD). Dysregulation of complement leads to excessive inflammation, direct damage to self-cells and propagation of injury. This is likely of particular relevance in the brain where inflammation is poorly tolerated and brain cells are vulnerable to direct damage by complement.
View Article and Find Full Text PDFBackground: In the brain as in other organs, complement contributes to immune defence and housekeeping to maintain homeostasis. Sources of complement may include local production by brain cells and influx from the periphery, the latter severely restricted by the blood brain barrier (BBB) in healthy brain. Dysregulation of complement leads to excessive inflammation, direct damage to self-cells and propagation of injury.
View Article and Find Full Text PDFEnter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!