Osteoarthritis (OA), defined as a long-term progressive joint disease, is characterized by cartilage impairment and erosion. In recent decades, magnolol, as a type of lignin extracted from Magnolia officinalis, has been proved to play a potent anti-inflammatory role in various diseases. The current research sought to examine the latent mechanism of magnolol and its protective role in alleviating the progress of OA in vivo as well as in vitro experimentations. In vitro, the over-production of Nitric oxide (NO), prostaglandin E2 (PGE2), cyclooxygenase-2 (COX-2), inducible nitric oxide synthase (iNOS), tumor necrosis factor alpha (TNF-α), and interleukin-6 (IL-6), induced by interleukin-1 beta (IL-1β), were all inhibited notably by magnolol in a concentration-dependent manner. Moreover, magnolol could also downregulate the expression of metalloproteinase 13 (MMP13) and thrombospondin motifs 5 (ADAMTS5). All these changes ultimately led to the deterioration of the extracellular matrix (ECM) induced by IL-1β. Mechanistically, magnolol suppressed the activation of PI3K/Akt/NF-κB pathway. Furthermore, a powerful binding capacity between magnolol and PI3K was also revealed in our molecular docking research. In addition, magnolol-induced protective effects in OA development were also detected in a mouse model. In summary, this research suggested that magnolol possessed a new therapeutic potential for the development of OA.

Subarachnoid hemorrhage (SAH) is a common complication of cerebral vascular disease. Hydrogen has been reported to alleviate early brain injury (EBI) through oxidative stress injury, reactive oxygen species (ROS), and autophagy. Autophagy is a programmed cell death mechanism that plays a vital role in neuronal cell death after SAH. However, the precise role of autophagy in hydrogen-mediated neuroprotection following SAH has not been confirmed. In the present study, the objective was to investigate the neuroprotective effects and potential molecular mechanisms of hydrogen-rich saline in SAH-induced EBI by regulating neural autophagy in the C57BL/6 mice model. Mortality, neurological score, brain water content, ROS, malondialdehyde (MDA), and neuronal death were evaluated. The results show that hydrogen-rich saline treatment markedly increased the survival rate and neurological score, increased neuron survival, downregulated the autophagy protein expression of Beclin-1 and LC3, and endoplasmic reticulum (ER) stress. That indicates that hydrogen-rich saline-mediated inhibition of autophagy and ER stress ameliorate neuronal death after SAH. The neuroprotective capacity of hydrogen-rich saline is partly dependent on the ROS/Nrf2/heme oxygenase-1 (HO-1) signaling pathway. The results of this study demonstrate that hydrogen-rich saline improves neurological outcomes in mice and reduces neuronal death by protecting against neural autophagy and ER stress.

Background: Primary brainstem hemorrhage (PBSH) is a life-threatening neurological condition associated with high mortality and disability rates. Stereotactic hematoma aspiration surgery has been explored as a treatment option, and postoperative brainstem function monitoring is considered important for patient management. Objective: This study aimed to evaluate the integration of minimally invasive stereotactic aspiration surgery with quantitative electroencephalography (qEEG) and transcranial Doppler (TCD) monitoring to assess brain function and improve predictive models for clinical outcomes in PBSH patients. Methods: We conducted a retrospective analysis of 34 PBSH patients admitted between December 2022 and October 2023. After applying exclusion criteria, 25 eligible patients underwent stereotactic aspiration surgery within 24–48 hours of symptom onset. Both qEEG and TCD monitoring were performed preoperatively and within 24 hours postoperatively. Changes in qEEG parameters and TCD-derived hemodynamic indices were analyzed to assess surgical safety and efficacy. Results: Stereotactic surgery was associated with higher rates of favorable outcomes at 90 days compared with the non-surgical group (68.75% vs. 11.11%, p = 0.01). Postoperative TCD parameters improved significantly, indicating better hemodynamic stability, though no correlation with mRS scores was found. qEEG analysis showed significant correlations between RBP δ% and mRS scores (ρ = 0.480, p = 0.015), and RBP α% (ρ = −0.456, p = 0.022). aEEG also correlated strongly with 90-day mRS scores (ρ = 0.544, p = 0.004). The combined model of hematoma volume, RBP α%, and aEEG showed the highest predictive accuracy (AUC = 0.865). Conclusion: This study suggests the prognostic value of qEEG and explores the utility of combining neurophysiological monitoring with stereotactic aspiration surgery. The integration of these tools may assist in prognostic assessment for PBSH patients; however, validation in larger prospective studies is required before clinical adoption.

INPLASY202380100 Application of Metagenomic Next-Generation Sequencing in the Diagnosis of Central Nervous System Infections after Craniotomy: A Systematic Review and Meta-Analysis Keywords: Metage…

Background: Holmes tremor (HT) is a rare motor disorder characterized by high-amplitude and low-frequency resting, intentional, and postural tremors. HT typically arises from disruptions in neural pathways, including the dopaminergic system. Its causes include cerebrovascular incidents, neoplasms, demyelination, and infections. Diagnosis involves thorough clinical, neurophysiological, and neuroimaging assessments. Our report details the clinical profile, neuroimaging and EEG results and levodopa treatment response of an HT patient after cerebral arteriovenous malformation (AVM) surgery. Case Report: A female patient who underwent AVM surgery developed head tremor and dystonia. Neuroimaging revealed left thalamus involvement. Video electroencephalography (EEG) revealed high-amplitude, low-frequency tremors. The patient responded well to levodopa treatment. Conclusions: Involuntary rhythmic or non-rhythmic movements are a primary clinical feature of HT. A differential diagnosis of epilepsy and HT can be achieved through neurophysiological monitoring, avoiding the overuse of antiepileptic drugs. Symptoms can be alleviated with levodopa intervention.