scholarly journals Healthcare Data-Based Prediction Algorithm for Potential Knee Joint Injury of Football Players

2021 ◽  
Vol 2021 ◽  
pp. 1-10
Author(s):  
Yue Yu ◽  
Zi Ye
Keyword(s):  
Knee Joint ◽  
Prediction Accuracy ◽  
Knee Injury ◽  
Knee Injuries ◽  
Prediction Algorithm ◽  
Football Players ◽  
Joint Injury ◽  
Healthcare Data ◽  
Knee Joint Injury ◽  
Prediction Systems

It is important to predict the potential harm to the knee joint in order to prevent football players from inflicting numerous injuries to the knee during activity. Numerous professionals have been drawn to this subject, and many viable prediction systems have been developed. Prediction of potential knee joint injury is critical to effectively avoid knee joint injury during exercise. The current prediction algorithms are mainly implemented through expert interviews, medical reports, and historical documents. The algorithms have problems with low prediction accuracy or precision values. There is a need to understand more knee injury factors and improve the prediction accuracy; hence, the intelligent prediction algorithm for potential injury of knee joints of football players is proposed in this paper. Firstly, the characteristics of the knee joint injury and the injury factors of the football players are gathered and analyzed. Then, the damage is predicted by the similarity measurement. The experimental results show that the proposed algorithm has higher prediction accuracy and shorter time. According to the findings of a survey that collected healthcare data, several key factors contribute to football knee injuries. To a degree, this algorithm can predict the likelihood of a football player’s knee injury.

scholarly journals Neutrophil Extracellular Traps Promote Joint Injury in Hemophilia

Blood ◽  
2021 ◽  
Vol 138 (Supplement 1) ◽  
pp. 990-990
Author(s):  
Tomasz W. Kaminski ◽  
Tomasz Brzoska ◽  
Egemen Tutuncuoglu ◽  
Margaret V. Ragni ◽  
Prithu Sundd
Keyword(s):  
Knee Joint ◽  
Board Of Directors ◽  
Research Funding ◽  
Knee Injury ◽  
Innate Immune ◽  
Sterile Inflammation ◽  
Advisory Committees ◽  
Joint Injury ◽  
Knee Joint Injury ◽  
Immune Pathways

Abstract Epidemiological evidence suggests that recurring episodes of joint-bleeding contribute to the development of hemophilic arthropathy (H) in 70-85% of hemophilia patients. Despite major advances in the treatment to prevent joint bleeding, HA continues to be a major morbidity affecting hemophilia patients and the etiological mechanism contributing to the progression of HA remains poorly understood. Recent evidence suggests that the accumulation of blood in the joints may lead to the release of erythrocyte-derived DAMPs (eDAMPs) such as heme and hemoglobin that can promote sterile inflammation, however, the innate immune pathways contributing to this pathophysiology remain unknown. In the study, we used a model of puncture-induced knee joint injury in FVIII-total knockout (F8TKO) mice and blood samples from hemophilia-A patients diagnosed with HA. Intravital multi-photon-excitation fluorescence intravital (in vivo) microscopy of injured synovium in live F8TKO or control mice was conducted to assess neutrophil-platelet aggregation and NETs generation in the knee-joint. Imaging-flow-cytometry and ELISA assays were used to estimate the number of circulating NETs in plasma of patients diagnosed with HA and mice after the knee-injury procedure. Scoring of the bleeding severity, histology, IHC and confocal imaging of joints were conducted to quantify the joint injury in mice. F8TKO but not control mice manifested knee-joint injury and severity of bleeding 5-days post knee-injury. Progression of knee-joint injury was associated with increased neutrophil accumulation and NETs shedding within the synovium of F8TKO mice. Circulating NETs were significantly abundant in the plasma of hemophilia patients diagnosed with HA and F8TKO mice following knee-injury but not plasma of control humans or mice. These findings are the first to suggest that NETs contribute to pathogenesis of HA in hemophilia. Currently, experiments are underway to identify the innate immune pathways that promote NETs shedding, leading to joint-damage in hemophilia. Disclosures Ragni: Takeda Therapeutics: Membership on an entity's Board of Directors or advisory committees; Bioverativ (Sanofi): Membership on an entity's Board of Directors or advisory committees; BioMarin Pharmaceutical: Membership on an entity's Board of Directors or advisory committees; Alnylam (Sanofi): Membership on an entity's Board of Directors or advisory committees; University of Pittsburgh: Research Funding; Spark Therapeutics: Membership on an entity's Board of Directors or advisory committees. Sundd: CSL Behring Inc: Research Funding; Novartis: Membership on an entity's Board of Directors or advisory committees, Research Funding; Bayer: Research Funding.

scholarly journals Neutrophil Extracellular Traps Promote Joint Injury in Hemophilia

Blood ◽  
2020 ◽  
Vol 136 (Supplement 1) ◽  
pp. 43-43
Author(s):  
Tomasz W. Kaminski ◽  
Tomasz Brzoska ◽  
Egemen Tutuncuoglu ◽  
Margaret V. Ragni ◽  
Prithu Sundd
Keyword(s):  
Knee Joint ◽  
Research Funding ◽  
Knee Injury ◽  
Joint Damage ◽  
Innate Immune ◽  
Confocal Imaging ◽  
Sterile Inflammation ◽  
Joint Injury ◽  
Knee Joint Injury ◽  
Immune Pathways

Hemophilic arthropathy (HA) is the predominant pathophysiology resulting from recurrent joint bleeding in individuals with hemophilia. HA leads to permanent joint damage, chronic pain and reduced quality of life. Despite major advances in the treatment to prevent joint bleeding, HA continues to be a major morbidity affecting hemophilia patients and the etiological mechanism contributing to the progression of HA remains elusive. Recent evidence suggests that joint-bleeding may promote the release of erythrocyte and tissue-derived damage-associated-molecular-pattern molecules (DAMPs) that can trigger the sterile inflammation in the joints, however, the innate immune pathways contributing to the development of HA remain unclear. Here, we used a model of knee joint injury-induced HA in FVIII-total knockout (F8TKO) mice and blood samples from hemophilia patients diagnosed with HA. In vivo multi-photon-excitation (MPE) fluorescence imaging of injured synovial cavity in live F8TKO or control mice was used to assess NETs formation within joint capsule. Imaging-flow-cytometry and ELISA assays were used to evaluate the number of circulating NETs in patients diagnosed with HA and mice with knee-injury. Scoring of the bleeding severity, histology, IHC and confocal imaging of joints were conducted to assess the joint injury in mice. F8TKO but not control mice manifested knee-joint injury and severity of bleeding 5-days post knee-injury. Progression of knee-joint injury was associated with increased neutrophil accumulation and NETs shedding within the synovium of F8TKO mice. Circulating NETs were significantly abundant in the plasma of hemophilia patients diagnosed with HA and F8TKO following knee-injury but not plasma of control humans or mice. These findings are the first to suggest that NETs contribute to pathogenesis of HA in hemophilia. Currently, experiments are underway to identify the innate immune pathways that promote NETs shedding, leading to joint-damage in hemophilia. Disclosures Ragni: Alnylam/Sanofi, ATHN, BioMarin, Bioverativ, Sangamo, Spark: Research Funding; Alnylam/Sanofi, BioMarin, Bioverativ, Spark: Consultancy; BioMarin: Consultancy, Research Funding; Bioverativ: Consultancy, Research Funding; Spark: Consultancy, Research Funding; Takeda: Research Funding; Sangamo: Consultancy, Research Funding; Alnylam Pharmaceuticals Inc., Baxalta/Takeda, BioMarin, Bioverativ, and Spark Therapeutics: Membership on an entity's Board of Directors or advisory committees; American Thrombosis Hemostasis Network: Other: Committee work; Baxalta/Takeda, CSL Behring, Genentech, a member of the Roche Group, OPKO Biologics, and Vascular Medicine Institute: Research Funding.

scholarly journals Nongenotoxic antibody-drug conjugate conditioning enables safe and effective platelet gene therapy of hemophilia A mice

2019 ◽  
Vol 3 (18) ◽  
pp. 2700-2711 ◽  
Author(s):  
Chunyan Gao ◽  
Jocelyn A. Schroeder ◽  
Feng Xue ◽  
Weiqing Jing ◽  
Yuanhua Cai ◽  
...  
Keyword(s):  
Gene Therapy ◽  
Knee Joint ◽  
Hemophilia A ◽  
Hematopoietic Cell ◽  
Antibody Drug Conjugate ◽  
Joint Injury ◽  
Drug Conjugate ◽  
Key Points ◽  
Knee Joint Injury ◽  
Antibody Drug

Key Points Hematopoietic cell–targeted antibody-drug conjugate preconditioning is highly effective for platelet gene therapy in hemophilia A mice. Platelet-specific FVIII gene therapy can effectively prevent a needle-induced knee joint injury in hemophilia A mice.

A Review of Current Management of Knee Hemarthrosis in the Non-Hemophilic Population

Cartilage ◽  
2020 ◽  
pp. 194760352094293
Author(s):  
Nikhil Potpally ◽  
Scott Rodeo ◽  
Paul So ◽  
Ken Mautner ◽  
Michael Baria ◽  
...  
Keyword(s):  
Knee Joint ◽  
The Body ◽  
Breakdown Product ◽  
Acute Management ◽  
Optimal Management ◽  
Current Management ◽  
Joint Injury ◽  
Joint Aspiration ◽  
Knee Joint Injury ◽  
Harmful Effects

The knee joint is one of the most frequently injured joints in the body, and the resulting injury may often lead to the presence of a bloody effusion, or hemarthrosis. The acute management of this condition can have long-lasting implications, and may ultimately result in the early onset of osteoarthritis in this population. Heme, a breakdown product of erythrocytes, and associated pro-inflammatory mediators, are known to have deleterious interactions with cartilage and synovium. The presence of blood in a joint following injury can precipitate these effects and accelerate the degenerative changes in the joint. Currently, there is no consensus on the optimal management of a traumatic knee joint injury with a hemarthrosis. Nontraumatic hemarthosis, seen most commonly in hemophilia patients, has a set of established guidelines that does not routinely recommend drainage of the joint. This article presents a rationale for joint aspiration to minimize the harmful effects of blood following traumatic hemarthrosis.

316 FE modeling for knee joint injury reconstruction

2006 ◽  
Vol 2006.55 (0) ◽  
pp. 143-144
Author(s):  
Kazutoshi NAKANO ◽  
Sota YAMAMOTO ◽  
Takayuki KUSHIDA ◽  
Eiichi TANAKA ◽  
Koji MIZUNO
Keyword(s):  
Knee Joint ◽  
Fe Modeling ◽  
Joint Injury ◽  
Knee Joint Injury
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