Introduction: Anterior cruciate ligament (ACL) rupture with concomitant damage to the medial collateral ligament (MCL) is frequently seen following knee trauma. Non-surgical treatment of the MCL lesion generally results in good internal healing, but surgery may be necessary depending on the location of the lesion, the severity, and the laxity.
Objectives: To determine outcomes following ACL reconstruction surgery when there is concomitant damage to the MCL compared to isolated ACL lesions, as assessed through a prospective, multi-center cohort study in France.
Materials And Methods: In this prospective, multi-center cohort study, patients who had a primary ACL lesion with or without concomitant damage to the MCL, and who had undergone ACL reconstruction surgery were included. Complications related to the surgery were evaluated prospectively (ACL re-rupture, contralateral rupture, reoperation), and functional scores were obtained until the last follow-up (subjective IKDC, Tegner, ACL-RSI, and SKV).
Results: A total of 722 patients were included in the study: 314 (43.5%) with an isolated ACL lesion and 408 (56.5%) with a combined ACL + MCL lesion. The ACL + MCL group had a significantly higher reoperation rate than the ACL group (7.4% versus 3.2%, p = 0.015). The ACL + MCL group also had mean IKDC and SKV scores at the last follow-up that were significantly poorer than the ACL group (p < 0.0001). High-grade MCL lesions (grade II or III) were identified in 18.2% of cases, and this was found to be predictive of poorer functional scores at the last follow-up. The mean IKDC score was significantly better when non-surgical MCL treatment was possible (p = 0.005). When MCL surgery was indicated, all of the functional scores were significantly better for ligament reinsertion surgery compared to ligament reconstruction.
Conclusion: For combined ACL + MCL lesions, the outcomes are poorer, with a higher reoperation rate and lower functional scores. For high-grade MCL lesions, the functional recovery is poorer, particularly when there are chronic lesions that require multi-ligament reconstruction.
Level Of Evidence: II; prospective cohort study.
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http://dx.doi.org/10.1016/j.otsr.2025.104194 | DOI Listing |
Handb Clin Neurol
March 2025
Institute of Neurology, Università Cattolica del Sacro Cuore, Fondazione Policlinico A. Gemelli, IRCCS, Rome, Italy. Electronic address:
Since several reviews have recently discussed the lateralization of emotions, this chapter will take into account the possible evolutionary meaning of this lateralization. The organization of the chapter will be based on the following steps. I will first propose that emotions must be considered as a complex adaptive system, complementary to the more phylogenetically advanced cognitive system.
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March 2025
Department of Pediatrics, Shanghai TCM-Integrated Hospital, Shanghai 200082, China. Electronic address:
Background And Objective: Neonatal hypoxic-ischemic encephalopathy (HIE) remains a critical challenge in perinatal medicine. This study aimed to elucidate the transcriptomic landscape, focusing on long non-coding RNAs (lncRNAs) expression patterns in the brain tissues of a neonatal rat model of HIE.
Methodology: We employed a modified Rice-Vannucci model to induce HIE in postnatal day 4 (P4) rats.
Explor Target Antitumor Ther
February 2025
Algoma District Cancer Program, Sault Area Hospital, Sault Ste. Marie, ON P6B 0A8, Canada.
Aim: Colorectal cancer is the most prevalent gastrointestinal malignancy with limited therapeutic options in the metastatic setting. The WNT/β-catenin/adenomatous polyposis coli (APC) pathway is commonly deregulated in the disease and presents a rational target for therapeutic exploitation.
Methods: The publicly available genomic data from the colorectal cancer cohort of the Cancer Genome Atlas (TCGA) were used to define groups of colorectal cancers with alterations in or other key genes of the WNT/β-catenin/APC pathway and to identify genomic characteristics of interest in each group.
Acta Neuropathol Commun
March 2025
Division of DNA Repair Research, Center for Neuroregeneration, Department of Neurosurgery, Houston Methodist Research Institute, Houston, TX, 77030, USA.
TDP-43 mislocalization and aggregation are key pathological features of amyotrophic lateral sclerosis (ALS)- and frontotemporal dementia (FTD). However, existing transgenic hTDP-43 WT or ∆NLS-overexpression animal models primarily focus on late-stage TDP-43 proteinopathy. To complement these models and to study the early-stage motor neuron-specific pathology during pre-symptomatic phases of disease progression, we generated a new endogenous knock-in (KI) mouse model using a combination of CRISPR/Cas9 and FLEX Cre-switch strategy for the conditional expression of a mislocalized Tdp-43∆NLS variant of mouse Tdp-43.
View Article and Find Full Text PDFSkelet Muscle
March 2025
Centro Científico y Tecnológico de Excelencia, Ciencia & Vida, 8580702, Santiago, Chile.
Background: Sarcoglycanopathies are muscle dystrophies caused by mutations in the genes encoding sarcoglycans (α, β, γ, and δ) that can destabilize the dystrophin-associated glycoprotein complex at the sarcolemma, leaving muscle fibers vulnerable to damage after contraction, followed by inflammatory and fibrotic responses and resulting in muscle weakness and atrophy. Two signaling pathways have been implicated in fibrosis and inflammation in various tissues: autotaxin/lysophosphatidic acid (ATX-LPA) and yes-associated protein 1/transcriptional co-activator with PDZ-binding motif (YAP/TAZ). LPA, synthesized by ATX, can act as a pleiotropic molecule due to its multiple receptors.
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