Mechanism Of Injury Research Articles

Development, calibration and validation of impact-specific cervical spine models: A novel approach using hybrid multibody and finite-element methods

Background and Objective:Spinal cord injuries can have a severe impact on athletes’ or patients’ lives. High axial impact scenarios like tackling and scrummaging can cause hyperflexion and buckling of the cervical spine, which is often connected with bilateral facet dislocation. Typically, finite-element (FE) or musculoskeletal-models are applied to investigate these scenarios, however, they have the drawbacks of high computational cost and lack of soft tissue information, respectively. Moreover, material properties of the involved tissues are commonly tested in quasi-static conditions, which do not accurately capture the mechanical behavior during impact scenarios. Thus, the aim of this study was to develop, calibrate and validate an approach for the creation of impact-specific hybrid, rigid body - finite-element spine models for high-dynamic axial impact scenarios. Methods:Five porcine cervical spine models were used to replicate in-vitro experiments to calibrate stiffness and damping parameters of the intervertebral joints by matching the kinematics of the in-vitro with the in-silico experiments. Afterwards, a five-fold cross-validation was conducted. Additionally, the von Mises stress of the lumped FE-discs was investigated during impact. Results:The results of the calibration and validation of our hybrid approach agree well with the in-vitro experiments. The stress maps of the lumped FE-discs showed that the highest stress of the most superior lumped disc was located anterior while the remaining lumped discs had their maximum in the posterior portion. Conclusion:Our hybrid method demonstrated the importance of impact-specific modeling. Overall, our hybrid modeling approach enhances the possibilities of identifying spine injury mechanisms by facilitating dynamic, impact-specific computational models.

Analysing lower limb motion and muscle activation in athletes with ankle instability during dual-task drop-jump

ABSTRACT This study investigates the impact of chronic ankle instability (CAI) on athletes’ lower extremity mechanics during bounce drop-jump landings with divided attention. Thirty Division I physical education voluntarily participated in the study. They performed two sets of bounce drop jumps: one set with a divided attention task and the other without. The obtained data were analysed using a paired t-test to compare the outcomes between the divided attention (DA) and non-divided attention (NDA) tasks. Athletes with CAI, during the DA task, displayed higher vertical landing forces, increased ankle inversion velocity, and greater range of motion of the ankle, knee, and hip in the frontal and transverse planes. They also exhibited insufficient neuromuscular preparation of the rectus femoris muscle. Notably, distinct kinematic alterations were observed in the ankle, knee, and hip joints regarding frontal and transverse lower-extremity kinematics. The findings suggest that athletes with CAI experience decreased activation of the rectus femoris muscle, which may impact their dynamic postural stability from pre-landing to ascending phases. Furthermore, the results indicate that individuals with CAI closely replicate the injury mechanisms encountered during a drop-jump landing task with divided attention. These insights offer valuable information about the real-time challenges faced by athletes with CAI.

The role of supplementation in traumatic brain injury among athletes and non-athletes population

Introduction: Traumatic brain injury (TBI) is one of the most common causes of death and long-term disability. The consequences following TBI can be persistent and cause life-long implications for survivors. Treatment of TBI may be complex and involve large monetary costs. The frequent injury mechanisms are traffic-related, falls, violence or sport-related accidents. Higher risk of brain injury and its complications indicate that people affected by brain trauma may benefit from the prophylactic and post-traumatic use of certain supplements both in the context of physical performance and in the event of potential injury. Aim of the Study: This narrative review examines the current literature of the role of supplementation before and after TBI and its effects on the patient's outcome. Materials and Methods: A comprehensive search was performed using PubMed and Google Scholar focusing on the literature published up to April 2024. The review included randomized controlled trials, meta-analyses, systematic reviews that focused on the use of creatine monohydrate, omega-3 fatty acids, magnesium and zinc in TBI and among the general population. Data of pathophysiology and epidemiology of TBI and safety profile of supplements were involved. Results: The evidence indicates that the role of supplementation with creatine, omega-3 PUFAs and zinc is important in mitigating secondary damage after TBI, as well as in protecting against damage if administered before injury. Conclusion: Because of the complex and multifactorial nature of the TBI more studies are required to constitute an effective nutrition-based strategy for reducing the cognitive and behavioral deficits associated with this injury. The evidence supporting multiple dietary components to improve a patient's outcome seems strong and the cost of its implementation is low. A group of particular interest that may benefit additionally are athletes who use dietary supplementation in their daily routine.

Cuboid fracture: surgical treatment, midterm follow-up, and management algorithm

Objectives: Describe the epidemiology of cuboid fracture, the mechanisms of injury and associated injuries, the progression to osteoarthritis, and propose a surgical management algorithm. Methods: A retrospective and descriptive study of patients with cuboid fractures operated on between 2009 and 2014. The variables analyzed were age, sex, mechanism of injury, classification, associated fractures, and osteoarthritis changes, among others. Results: Twenty-seven patients were included: 19 men and eight women. The mean age was 41.3 years (range 25 - 62). The mean followup was 3.3 years. The mechanisms of injury were motor vehicle accidents and falls from height. Among the patients, 44.4% had lateral column shortening, and 81.5% involved calcaneal cuboid articular surface. Cuboid locking plates were used in 15 patients, and single screw fixation was used in four patients. Three patients required a bone graft. Degenerative changes were observed in calcaneocuboid and cuboid-metatarsal joints. Conclusions: Cuboid fracture is an uncommon injury. In general, the injuries are caused by high-energy accidents. In our study, 40.7% of patients had an injury to the medial column. It is recommended the use of a cuboid locking plate for comminuted fractures, screw fixation for simple fractures, and a bridging plate or external fixation can be considered for most complex cases. Level of Evidence IV; Retrospective Case Series.

Epidemiology of High-Energy Distal Radius Fractures.

Background: High-energy distal radius fractures have not been as well studied as the more common osteoporotic fractures. Differences between these two groups of fractures have implications on the prevention and clinical management of such injuries. Methods: A retrospective review was conducted of all patients in our institution who presented with distal radius fractures within the period of a year. Demographic data, injury mechanism, fracture classification, associated injuries and work-related status were obtained and analysed. Results: High energy fractures made up 27.1% of the cases. Falls from height were the most common cause, followed by motor vehicle accidents. These high-energy fractures were more commonly seen in males, younger patients (average age 41 vs. 61 years), and in workplace accidents. These injuries were also more likely to be bilateral and associated with an additional ipsilateral upper extremity injury. The high-energy group was also more likely to have an AO type B fracture. Conclusions: A substantial proportion of distal radius fractures seen in our population are high-energy injuries. Their contrasting patient and injury profiles suggest that they should be considered separately from osteoporotic fractures. Level of Evidence: Level IV (Therapeutic).

Zearalenone induces liver injury in mice through ferroptosis pathway

Throughout the world, some foods and feeds commonly consumed by humans and animals are inadvertently contaminated with mycotoxins. Zearalenone (ZEA) is a typical environmental/food contaminant that can cause varying degrees of damage to the body, such as reproductive toxicity, hepatotoxicity, immunotoxicity, etc. It poses a serious threat to the living environment and human and animal health. Increasing evidence shows that mycotoxin-induced organ damage may be closely related to ferroptosis. However, the mechanism of ZEA-induced liver injury is still not fully understood. Therefore, this study aimed to explore whether ZEA can trigger ferroptosis in the liver and cause liver injury. This study was conducted by establishing in vivo and in vitro ZEA exposure models. The results showed that ZEA exposure led to typical liver injury indicators. ZEA inhibited the Nrf2/keap1 antioxidant signaling pathway, aggravated the oxidative stress response, and inhibited the body's antioxidant function. Additionally, it was found that ZEA can aggravate lipid peroxidation by blocking the system Xc−/GSH/GPX4 axis, upregulating the protein expression of ACSL4, and affecting the import, storage, and export of iron ions, thereby inducing iron ion metabolism disorders. A combination of multiple factors induces ferroptosis in mouse liver and AML12 cells. Pretreatment with deferoxamine, an inhibitor of ferroptosis, can alleviate ferroptosis damage induced by ZEA, indicating the crucial role of ferroptosis in cell damage caused by ZEA. This study deeply explores the hepatic ferroptosis pathway induced by ZEA, provides a new theoretical basis for ZEA-induced hepatotoxicity, and offers new insights for exploring potential treatment strategies.

Meniscus Tears in Climbing - a Triviality or Serious Concern?

Introduction In the past few years, the popularity of climbing and the number of its new recreational enthusiasts increased. It became clear that there are more types of trauma than finger injuries that should be commonly associated with the sport. This overview focuses on meniscus tears as a prevalent underestimated complaint of climbers. Aim of the studyWe aim to bring attention to meniscus lesions and deal with mechanisms of knee injury in climbing while considering the current views on the structure, function, types of lesions, treatment methods, and results in light of topical literature. Materials and methodsThe methodology for the literature search involved using the keywords: ''meniscus tears'', ''climbing injury'', ''bouldering'', ''arthroscopy'', and ''meniscus repair''. The phrases were searched in the PubMed and Google Scholar databases. ConclusionsWe concluded that climbers should recognise acute and chronic meniscus lesions as a concern requiring training breaks, possibly further diagnosis, and adequate treatments. Moreover, awareness of the risk of this type of injury in climbing should be raised, and preventive action should be taken to limit the number of new cases.

Man on the Mound: Pictures of a Pitcher in Pain.

Description Atraumatic ball thrower's humerus fracture is an uncommon, and poorly understood injury pattern. The majority of these cases are seen in untrained and younger individuals. A missed diagnosis could severely impact a patient's quality of life, as management is operative in most cases. Here, we present the case of a young patient, suffering an atraumatic "ball thrower's" fracture. We present images of this exceedingly rare injury pattern and showcase original artwork with a proposed mechanism of injury.

Histological and Molecular Biological Changes in Canine Skin Following Acute Radiation Therapy-Induced Skin Injury.

Radiation therapy is a crucial cancer treatment, but it can damage healthy tissues, leading to side effects like skin injuries and molecular alterations. This study aimed to elucidate histological and molecular changes in canine skin post-radiation therapy (post-RT) over nine weeks, focusing on inflammation, stem cell activity, angiogenesis, keratinocyte regeneration, and apoptosis. Four male beagles received a cumulative radiation dose of 48 Gy, followed by clinical observations, histological examinations, and an RT-qPCR analysis of skin biopsies. Histological changes correlated with clinical recovery from inflammation. A post-RT analysis revealed a notable decrease in the mRNA levels of Oct4, Sox2, and Nanog from weeks 1 to 9. VEGF 188 levels initially saw a slight increase at week 1, but they had significantly declined by week 9. Both mRNA and protein levels of COX-2 and Keratin 10 significantly decreased over the 9 weeks following RT, although COX-2 expression surged in the first 2 weeks, and Keratin 10 levels increased at weeks 4 to 5 compared to normal skin. Apoptosis peaked at 2 weeks and diminished, nearing normal by 9 weeks. These findings offer insights into the mechanisms of radiation-induced skin injury and provide guidance for managing side effects in canine radiation therapy.

Optimizing vehicle Front-End structure for e-bike rider Safety: An advanced Multi-Objective approach using injury prediction models

A multi-objective optimization method based on an injury prediction model is proposed to address the increasingly prominent safety issues for e-bike riders in Chinese road traffic. This method aims to enhance the protective effect of vehicle front-end for e-bike riders by encompassing a broader range of test scenarios. Initially, large-scale rider injury response data were collected using automated Madymo simulations. A machine learning model was then trained to accurately predict the risk of rider injury under varied crash conditions. Subsequently, this model was integrated into a multi-objective optimization framework, combined with multi-criteria decision analysis, to effectively evaluate and rank various design alternatives on the Pareto frontier. This process entailed a comparative analysis of the design in a baseline scenario before and after optimization, focusing on both kinematic and injury responses of riders. Through detailed injury mechanism analysis, key design variables such as the height of the hood front and the width of the bumper were identified. This led to the proposal of specific optimization strategies for these structural parameters. The results from this study demonstrate that the proposed optimization method not only guides the design process accurately and efficiently but also balances the injury risks across different body parts. This approach significantly reduces the injury risk for riders in car-to-e-bike collisions and provides actionable insights for vehicle design enhancements.

Integration of proteomics and metabolomics analysis investigate mechanism of As-induced immune injury in rat spleen

Arsenic (As) is a widespread metalloid and human carcinogen found in the natural environment, and multiple toxic effects have been shown to be associated with As exposure. As can be accumulated in the spleen, the largest peripheral lymphatic organ, and long-term exposure to As can lead to splenic injury. In this study, a Sprague-Dawley (SD) rat model of As-poisoned was established, aiming to explore the molecular mechanism of As-induced immune injury through the combined analysis of proteomics and metabolomics of rats’ spleen. After feeding the rats with As diet (50 mg/kg) for 90 days, the spleen tissue of the rats in the As-poisoned group was damaged, the level of As was significantly higher than that of the control group (P < 0.001), and the level of inflammatory cytokine interleukin-6 (IL-6) was decreased (P < 0.01). Proteomics and metabolomics results showed that a total of 134 differentially expressed proteins (DEPs) (P < 0.05 and fold change > 1.2) and 182 differentially expressed metabolites (DEMs) (VIP >1 and P < 0.05) were identified in the spleens of the As poisoned group compared to the control group (As/Ctrl). The proteomic results highlight the role of hypoxia-inducible factors (HIF), natural killer cell mediated cytotoxicity, and ribosomes. The major pathways of metabolic disruption included arachidonic acid (AA) metabolism, glycerophospholipid metabolism and folate single-carbon pool. The integrated analysis of these two omics suggested that Hmox1, Stat3, arachidonic acid, phosphatidylcholine and leukotriene B4 may play key roles in the mechanism of immune injury to the spleen by As exposure. The results indicate that As exposure can cause spleen damage in rats. Through proteomic and metabolomic analysis, the key proteins and metabolites and their associated mechanisms were obtained, which provided a basis for further understanding of the molecular mechanism of spleen immune damage caused by As exposure.

Polyfracture and Cranial Injuries Drive the Cost and Inpatient Burden of Zygoma Fractures.

Facial trauma makes up a significant number of emergency room visits, with morbidity costs in excess of 1 billion dollars each year. Few studies have evaluated the economic outcomes of management and inpatient burden of facial trauma, most focusing solely on the mandible and isolated midface fractures. The authors aim to evaluate characteristics associated with increased cost and length of hospitalization of zygoma fracture management. Cross-sectional study. Level 1-trauma academic medical center. Patients with zygoma fractures who presented to our institution from 2008 to 2021. Demographics, injury mechanisms, associated injuries, treatment information, and associated costs were collected. Univariate and multivariate analyses were performed to identify the patient and fracture characteristics associated with increased cost and length of hospitalization. Our 14-year experience identified 689 patients with zygoma fractures who presented from 2008 to 2021. Seventy percent were male, and 40% occurred in Caucasian patients. The mean cost, adjusted for inflation, was $21,799.34, and the mean length of hospitalization was 5.5 days. Four or more fractures, associated cranial or intracranial injuries, and length of stay were associated with significantly higher cost, and 4 or more fractures, associated cranial or intracranial injuries, and female gender were associated with significantly longer length of hospitalization. This study represents one of the largest comprehensive databases of zygoma fractures and one of the first to provide a descriptive cost and inpatient burden analysis. To improve outcomes and reduce hospital cost and inpatient burden, protocols should be implemented to address the factors that the authors identified as contributing to increased cost and length of hospitalization.

Glucocorticoid alleviates hypothalamic nerve injury via remodeling HPA axis homeostasis in stressed rats

Excessive stress can exceed the adjustment ability of body and cause injury and dysfunction, while elucidation of the mechanism and prevention measures of stress-related injury are still insufficient. The present study was to observe the effect of glucocorticoid (GC) on stress-induced hypothalamic nerve injury and elucidate the potential mechanism. The present study intended to establish a chronic restraint stress rat model for follow-up study. Open field test and elevated plus maze test were used to observe behavioral changes of stress rats; Enzyme-linked immunosorbent assay (ELISA) was used to detect changes in the levels of hypothalamus-pituitary-adrenal (HPA) axis-related hormones and inflammatory factors in hypothalamus; toluidine blue staining was used to observe pathological changes of hypothalamus. The results showed that stress rats showed obvious anxiety-like behaviors, the levels of HPA axis-related hormones and inflammatory factors showed abnormal fluctuations, and morphological results showed significant nerve injury in hypothalamus. Low-dose GC treatment significantly improved behavioral changes, alleviated hypothalamic nerve injury, and restored hypothalamic levels of inflammatory factors, serum levels of GC, corticotropin-releasing hormone (CRH), and adrenocorticotropic hormone (ACTH) and GC level in adrenal cortex of stressed rats, while GC receptor (GR) inhibitor, CRH receptor inhibitor, and adrenalectomy reversed the ameliorative effects of low-dose GC. Our study clarified that low-dose GC can restore stress coping ability by reshaping the homeostasis of the HPA axis, thus alleviating behavioral abnormalities and hypothalamic nerve injury in stressed rats.

Endoplasmic reticulum stress promotes oxidative stress, inflammation, and apoptosis: A novel mechanism of citrinin-induced renal injury and dysfunction

Citrinin (CTN) has been reported to induce renal failure and structural damage, but its nephrotoxic effects and mechanisms are not fully understood. Therefore, we established a model by orally administering CTN (0, 1.25, 5, or 20 mg/kg) to mice for 21 consecutive days. Histological and biochemical analyses revealed that CTN caused structural damage to renal tubules, increased inflammatory cell infiltration, and elevated levels of serum markers of renal function (creatinine, urea, and uric acid). Moreover, mRNA transcript levels of the inflammatory factors TNF-α, IL-1β, and IL-6 were increased, indicating the occurrence of an inflammatory response. Furthermore, exposure to CTN induced renal oxidative stress by decreasing antioxidant GSH levels, antioxidant enzyme (SOD, CAT) activities, and increasing oxidative products (ROS, MDA). In addition, CTN increased the expression of proteins associated with endoplasmic reticulum (ER)stress and apoptotic pathways. ER stress has been shown to be involved in regulating various models of kidney disease, but its role in CTN-induced renal injury has not been reported. We found that pretreatment with the ER stress inhibitor 4-PBA (240 mg/kg, ip) alleviated CTN-induced oxidative stress, NF-κB pathway mediated inflammatory response, and apoptosis. Interestingly, 4-PBA also partially alleviated renal structural damage and dysfunction. Thus, ER stress may be a novel target for the prevention and treatment of CTN-induced renal injury.

Placental lesions in systemic lupus erythematosus pregnancies associated with small for gestational age infants.

Up to a quarter of pregnant individuals with systemic lupus erythematosus (SLE) have small for gestational age (SGA) infants. We aimed to characterize placental pathology associated with SGA infants in SLE. We retrospectively analyzed SLE deliveries with placental analysis at UCSD from 11/2018-10/2023, comparing SLE pregnancies resulting in SGA to those that did not, and additionally, to matched pregnancies with SGA but without SLE. Placental analysis was available only for 28/70 (40%) SLE deliveries, which had high rates of adverse outcomes (75%). All exhibited at least one histopathologic abnormality. Key findings distinguishing 12 SLE placentas resulting in SGA infants (vs.16 without) included small placental disc for gestational age (100% vs 56%, p= 0.01), placental disc infarct (50% vs 6%, p= 0.02), and increased perivillous fibrin deposition (PVFD, 58% vs 0%, p= 0.001). All seven SLE placentas with increased PVFD resulted in SGA infants. Compared with matched non-SLE pregnancies with SGA (n = 36), the only distinguishing placental lesion was a higher prevalence of increased PVFD in SLE-associated SGA (58% vs 22%, p= 0.03). The higher prevalence of increased PVFD in placentas of SLE-associated SGA may indicate a specific mechanism of placental injury leading to SGA in this context. Thus, its presence, particularly in context of SGA, should prompt providers to screen for an underlying autoimmune disease, including SLE. Systematic placental examination in context of SLE and associated autoimmune diseases could help evaluate responses to existing therapies, comparative studies of novel therapies, and correlation to adverse outcomes.

Immune Checkpoint Inhibitors in Cancer Treatment and Incidence of Pancreatitis.

Immune checkpoint inhibitors (ICIs) are an approved therapy for the management of various advanced neoplasms. Limited reviews focus on the influence of this therapy resulting in pancreatitis. This review discusses the relationship between ICIs and their effects on the pancreas, including the incidence of pancreatitis, immunotherapy, programmed cell death 1 (PD-1) receptors, driver mutations, programmed death ligand 1 (PD-L1), and immune-related adverse events. Additionally, it focuses on the clinical presentations, diagnosis, case studies, and mechanisms by which ICIs activate different pathways to cause pancreatitis. We conducted a comprehensive literature search using PubMed, Cochrane Library, and Google Scholar databases to identify relevant studies on ICI-associated pancreatitis. The review explores the incidence and epidemiology of ICI-induced pancreatitis, its clinical presentation, diagnostic criteria, and management strategies.The overall incidence of ICI-induced pancreatitis is estimated at 1-2%, with higher rates observed in combination therapy. Clinical presentations range from asymptomatic enzyme elevations to severe pancreatitis. Diagnosis relies on a combination of clinical symptoms, elevated pancreatic enzymes, and imaging findings, with MRI and endoscopic ultrasound showing promise in early detection. Management strategies include IV fluid administration, pain control, and nutritional support. The efficacy of corticosteroids remains controversial, and alternative immunosuppressants are being explored for steroid-refractory cases. Long-term monitoring is crucial due to the risk of chronic pancreatitis and pancreatic insufficiency. This review highlights the need for further research to elucidate the exact mechanisms of ICI-associated pancreatic injury, develop predictive biomarkers, and refine treatment protocols. As ICI use continues to expand, a thorough understanding of this adverse event is essential for optimizing patient care and outcomes in cancer immunotherapy.

Effects of vitamin D deficiency on chronic alcoholic liver injury

Vitamin D deficiency (VDD) has been found among alcoholics. However, little is known about the effect of VDD on alcoholic liver disease and the molecular mechanisms remain unclear. The aim of the current study was to evaluate whether vitamin D was deficient among patients with alcoholic fatty liver disease (AFLD) and the effect of VDD on chronic alcoholic liver injury and possible molecular mechanisms in mice. Our results found that lower 25-hydroxyvitamin D [25(OH)D] concentrations in patients with AFLD. And further analysis found that 25(OH)D is a protective factor in patients with AFLD. Mice experiments indicated that VDD can alter the composition of gut microbiota, down-regulate the protein levels of intestinal tight junction protein Occludin and E-cadherin, up-regulate the expression of inflammatory cytokines (tnf-α, il-1β, il-6, il-8, ccl2, il-10) in liver and colon tissue. And further exacerbated the protein levels of p65,P-IκB,P-p65 in alcoholic liver injury mice. In conclusion, VDD aggravates chronic alcoholic liver injury by activating NF-κB signaling pathway.

Jun-activated SOCS1 enhances ubiquitination and degradation of CCAAT/enhancer-binding protein β to ameliorate cerebral ischaemia/reperfusion injury.

This study investigates the molecular mechanisms behind ischaemia/reperfusion (I/R) injury in the brain, focusing on neuronal apoptosis. It scrutinizes the role of the Jun proto-oncogene in apoptosis, involvement of SOCS1 in neural precursor cell accumulation in ischaemic regions, and the upregulation of C-EBPβ in the hippocampus following I/R. Key to the study is understanding how Jun controls C-EBPβ degradation via SOCS1, potentially offering new clinical treatment avenues for I/R. Techniques such as mRNA sequencing, KEGG enrichment analysis and protein-protein interaction (PPI) in mouse models have indicated involvement of Jun (AP-1) in I/R-induced cerebral damage. The study employs middle cerebral artery occlusion in different mouse models and oxygen-glucose deprivation/reoxygenation in cortical neurons to examine the impacts of Jun and SOCS1 manipulation on cerebral I/R injury and neuronal damage. The findings reveal that I/R reduces Jun expression in the brain, but its restoration lessens cerebral I/R injury and neuron death. Jun activates SOCS1 transcriptionally, leading to C-EBPβ degradation, thereby diminishing cerebral I/R injury through the SOCS1/C-EBPβ pathway. These insights provide a deeper understanding of post-I/R cerebral injury mechanisms and suggest new therapeutic targets for cerebral I/R injury. KEY POINTS: Jun and SOCS1 are poorly expressed, and C-EBPβ is highly expressed in ischaemia/reperfusion mouse brain tissues. Jun transcriptionally activates SOCS1. SOCS1 promotes the ubiquitination-dependent C-EBPβ protein degradation. Jun blunts oxygen-glucose deprivation/reoxygenation-induced neuron apoptosis and alleviates neuronal injury. This study provides a theoretical basis for the management of post-I/R brain injury.

Demographic and Injury Characteristics as Potential Risk Factors for Anterior Cruciate Ligament Injuries: A Multicentric Cross-Sectional Study.

Background: Anterior cruciate ligament (ACL) injuries are prevalent and can have debilitating consequences, with various factors potentially influencing their occurrence. This multicentric study aimed to comprehensively analyze the epidemiological characteristics of ACL injuries. We hypothesized that specific patient characteristics, such as age, sex, body mass index (BMI), and sports involvement, would be associated with distinct injury patterns and risk profiles. Methods: This cross-sectional study analyzed the medical records of 712 patients aged 15-60 diagnosed with ACL rupture. Data on demographics, injury mechanisms, associated injuries, graft type, and sports involvement were collected. Results: The majority of patients were male (93.1%), aged 15-30 years (80.2%), and overweight (66.7%). Autografts were the predominant graft choice (96.07%). Associated injuries were present in 79.5% of cases, with medial meniscus ruptures being the most common (37.36%). Sports-related (49.3%) and non-sports-related (50.7%) injuries were nearly equal, with non-contact injuries more prevalent (71.1%). In the sports-related subgroup, associated injuries emerged as a significant risk factor for ACL rupture (p = 0.014, OR = 1.596, 95% CI: 1.101-2.314), whereas non-contact mechanisms showed borderline significance (OR = 0.75, p = 0.09). Moreover, younger athletes were more susceptible to sports-related injuries (p = 0.024), with football being the primary sport involved. Conclusions: This study identified a high prevalence of concomitant injuries with ACL injury, which increased the risk of ACL injury, particularly in sports-related cases. Age-related differences in injury patterns highlight the need for age-appropriate preventive measures, especially for younger athletes participating in high-risk sports. This underscores the need for comprehensive injury assessment, targeted prevention strategies, and optimized clinical management approaches tailored to different populations' specific characteristics and risks.

Retraction Note: Mechanism of arterial injury exacerbated by hyperhomocysteinemia in spontaneously hypertensive rats

Retraction Note: Mechanism of arterial injury exacerbated by hyperhomocysteinemia in spontaneously hypertensive rats