Kai Kang

Background: Many studies have shown that hypoplasia of knee bone morphology is related to the morphological features of the discoid lateral meniscus (DLM). However, few studies have focused on hypoplasia of tibial eminence morphology in juvenile patients with complete DLM. The purpose of this study was to determine the relationship between tibial eminence morphology characteristics and complete DLM in juvenile patients. Methods: The DLM group comprised 34 juvenile patients with complete DLM, and the control group comprised 34 juvenile individuals, each with a normal lateral meniscus based on magnetic resonance imaging (MRI) findings. All parameters, including tibial width (TW), tibial eminence width (TEW), the height of the lateral tibial spine (HLTS), the height of the medial tibial spine (HMTS), lateral slope angle of the lateral tibial eminence (LSALTE), lateral slope angle of the medial tibial eminence (LSAMTE), tibial eminence width ratio (TEWR), height of the lateral tibial spine ratio (HLTSR), and the height of the medial tibial spine ratio (HMTSR), were recorded using coronal MR images. Statistical analyses were used to determine the differences between the two groups and whether differences were significant. Results: The TEW and TEWR were significantly greater (P < 0.05), and LSALTE and LSAMTE were significantly smaller (P < 0.05) in patients in the DLM group than in participants in the control group. Receiver operating characteristic (ROC) analysis revealed that a larger TEW, above 13.4 mm, was associated with complete DLM, with a sensitivity of 77.0% and specificity of 88.2%, and a larger TEWR, above 19.7%, was associated with complete DLM, with a sensitivity of 76.5% and specificity of 91.2%. Conclusions: MR imaging can be used to diagnose tibial eminence hypoplasia in juvenile patients with complete DLM. Additionally, TEW and TEWR could help clinicians screen for complete DLM in juvenile patients.

Ischemic stroke, a cerebrovascular disease worldwide, triggers a cascade of pathophysiological events, including blood‐brain barrier (BBB) breakdown. Brain microvascular endothelial cells (BMECs) play a vital role in maintaining BBB function. The injury of BMECs may worsen neurovascular dysfunction and patients’ prognosis. Therefore, uncover the principal molecular mechanisms involved in BBB disruption in stroke becomes pressing. The endocannabinoid system (ECS) has been implicated in increasingly physiological functions, both in neurometabolism and cerebrovascular regulation. Modulating its activities by the fatty acid amide hydrolase (FAAH) shows anti‐inflammatory characteristics. Andrographolide (AG), one Chinese herbal ingredient, has also attracted attention for its role in immunomodulatory and as a therapeutic target in BBB disorders. Recently, the FAAH inhibitor URB597 and AG have important regulatory effects on neuronal and vascular cells in ischemia. However, the effects of URB597 and AG on BMEC permeability and apoptosis in oxygen‐glucose deprivation (OGD) and the underlying mechanisms remain unclear. To address these issues, cultured BMECs (bEnd.3 cells) were exposed to OGD. The cell viability, permeability, tube formation, and apoptosis were assessed following treatment with URB597, AG, and cotreatment. Mitochondrial membrane potential (MMP), reactive oxygen species (ROS), superoxide dismutase (SOD), catalase (CAT), malondialdehyde (MDA), proinflammatory factors, tight junction (TJ) proteins, and oxidative stress‐mediated Nrf2 signaling were also investigated. Results revealed that OGD broke the endothelial barrier, cell viability, MMP, and tube formation, which was reversed by URB597 and AG. OGD‐induced enhancement of ROS, MDA, and apoptosis was reduced after drug interventions. URB597 and AG exhibited antioxidant/anti‐inflammatory and mitochondrial protective effects by activating Nrf2 signaling. These findings indicated that URB597 and AG protect BMECs against OGD‐induced endothelial permeability impairment and apoptosis by reducing mitochondrial oxidative stress and inflammation associated with activation of Nrf2 signaling. URB597 and AG showing the vascular protection may have therapeutic potential for the BBB damage in ischemic cerebrovascular diseases.