The Second People's Hospital of Hunan Province

To compare the biomechanical stability between two different external fixation methods (locked steel plates versus external fixation frame) for the treatment of A1b tibial fractures based on finite element analysis, and to provide theoretical reference for clinical application.

Based on CT data of the left tibia from a healthy male volunteer, a normal three-dimensional (3D) tibial model was constructed using modeling software, which was further derived into a A1b tibial fracture model. Then, On the basis of the fracture model constructed above, the finite element models of locking compression plate and unilateral external fixator were fixed respectively. Further, 4 different test conditions (i.e., 4-point bending, axial compression, clockwise torsion, and counterclockwise torsion) were simulated under the same loading and constraint conditions for both models, in order to comparatively evaluate the equivalent peak stress and peak overall displacement of the fracture site between the two methods.

From the experimental data corresponding to the maximum load under 4 different test conditions, it was found that the peak stress of tibia and the equivalent peak stress of fractured tibia with external fixation was roughly ranged 49.16-269.59 MPa and 34.99-559.58 MPa in the two fixation methods under various test conditions. Overall, external fracture fixation with locked steel plates showed a greater equivalent peak stress and a smaller peak overall tibial displacement than that with external fixation frame did.

Locked steel plates may be superior external fixation frame in terms of biomechanical properties in the treatment of A1b tibial fractures, and can be used as an alternative option for patients who cannot tolerate external fixation frame.

The high prevalence of non-alcoholic Fatty Liver Disease (NAFLD), a chronic progressive disease characterized by hepatic steatosis, poses a serious burden to human health. Depression and NAFLD share some common pathogenic mechanisms, and patients with depression are at an increased risk of NAFLD. The drug mirtazapine is commonly used in the treatment of depression, but it can also cause liver damage. However, whether mirtazapine induces or aggravates NAFLD remains uncertain. Thus, we evaluated the risk factors for NAFLD in patients with depression and the effects of mirtazapine on NAFLD in vitro.

Inpatients diagnosed with depression at the Second Xiangya Hospital of Central South University between 2019 and 2022 were included in this study, and NAFLD was determined using an abdominal ultrasound examination. The risk factors for the development of NAFLD in patients with depression were analyzed using logistic regression analysis. AML-12 and MIHA cell lines were used to observe the effects of mirtazapine on NAFLD using oil red O staining. RT-qPCR and Western blotting were used to explore the molecular mechanism behind NAFLD development induced by mirtazapine.

Logistic regression analysis showed that older age, use of mirtazapine or fluoxetine, longer duration of antidepressant use, and combined hyperlipidemia or T2DM were risk factors for NAFLD in patients with depression. In vitro experiments revealed a subsequent increase in the content of intracellular lipid droplets as mirtazapine concentration increased. Mechanistic studies showed that mirtazapine increased the expressions of TLR4, MyD88, IFN-γ, IL-1β, IL-6, and TNF-α mRNA in hepatocytes and the expressions of TLR4, MyD88, and p-NF-κB-p65 proteins in a dose-dependent manner.

Age, antidepressant type, duration of antidepressant use, and comorbidities could be risk factors for NAFLD in patients with depression. Furthermore, mirtazapine can cause steatosis in both AML-12 and MIHA cell lines and may promote the development of NAFLD through the TLR4/MyD88/NF-κB signaling pathway. This study lays a solid foundation for further research on depression and NAFLD and can contribute to the prevention and treatment of these two diseases.

Insomnia is a common sleep disorder that severely impacts health and quality of life. Although music therapy is a widely used non-pharmacological treatment for sleep improvement, its lack of personalization limits its effectiveness.

We proposed a novel EEG neurofeedback intervention for sleep-aiding music therapy. A sleep-aiding style transfer model was developed to convert traditional five-element music into a sleep-aiding style. Subsequently, we established a neurofeedback framework linking an EEG parameter, the sleep state, and musical features. Leveraging the EEG alpha/theta power ratio, our system dynamically adjusted the tempo and volume of sleep-aiding five-element music in real time.

EEG neurofeedback intervention significantly improved ISI, PSQI, and sleep latency compared with the non-neurofeedback intervention. Notably, potential biomarkers were identified: reduced prefrontal-parietal functional connectivity in the alpha band during wakefulness (W) and increased functional connectivity from the central region to the central, occipital, and temporal regions in the theta band during light sleep (N1).

These findings highlight the potential of personalized, closed-loop neurofeedback music as an effective non-pharmacological intervention for insomnia. By dynamically adapting music parameters based on real-time EEG, this approach offers a novel method for optimizing sleep regulation and improving treatment outcomes.