Matrine induces hepatocellular carcinoma apoptosis and represses EMT and stemness through microRNA-299-3p/PGAM1 axis.

This study explored the impacts of matrine on hepatocellular carcinoma (HCC) cell growth, metastasis, epithelial-mesenchymal transition (EMT), and stemness through regulating the microRNA (miR)-299-3p/phosphoglycerate mutase 1 (PGAM1) axis. The association between miR-299-3p expression with the prognosis of HCC patients was studied. miR-299-3p and PGAM1 sequences were transfected into matrine-treated HCC cells, and cell proliferation, invasion, apoptosis, and stemness were detected, as well as protein expression of EMT- and stemness-related makers. The targeting relationship between miR-299-3p and PGAM1 was identified. Matrine elevated miR-299-3p expression, repressed proliferation, invasion, and anti-apoptosis of HCC cells, and constrained EMT and stemness in vitro. PGAM1 was a target of miR-299-3p. Repression of PGAM1 rescued the effects of miR-299-3p downregulation on HCC cells. Matrine stimulates HCC cell apoptosis and represses the process of EMT and stemness through the miR-299-3p/PGAM1 axis.

Study of Trunk Morphological Imbalance and Rehabilitation Outcome of Adolescent Idiopathic Scoliosis with Intelligent Medicine.

In recent years, artificial intelligence technology has been widely used in various medical fields to effectively assist physicians in patient treatment operations. In this paper, we design and implement a deep biblical network model-based orthotic design for adolescent idiopathic scoliosis to quickly and effectively assist physicians in designing orthotics for adolescent idiopathic scoliosis. A fuzzy set is used to express the knowledge of adolescent idiopathic scoliosis orthosis design, and a fuzzy reasoning based on the confidence level is implemented. Finally, the efficiency of the design of adolescent idiopathic scoliosis orthoses was improved by 50% through two cases of adolescent idiopathic scoliosis patients, and the deviation rate between the inference value and the actual operation value of the domain experts was less than 10%.

Effect of Early Cognitive Training Combined with Aerobic Exercise on Quality of Life and Cognitive Function Recovery of Patients with Poststroke Cognitive Impairment.

Objective: To explore the effect of early cognitive training combined with aerobic exercise on quality of life (QOL) and cognitive function recovery of patients with poststroke cognitive impairment (PSCI). Methods: Ninety PSCI patients treated in our hospital from April 2019 to April 2020 were selected as the subjects and were divided into the experimental group (EG) and control group (CG) according to the admission order, with 45 cases each. Patients in CG received conventional health education combined with rehabilitation training, and those in EG accepted early cognitive training combined with aerobic exercise so as to evaluate the clinical effect of different intervention modes on PSCI patients. Results: Compared with CG after intervention, EG obtained an obviously higher Stroke Specific Quality of Life scale (SS-QOL) score, Montreal Cognitive Assessment (MoCA) score, Barthel Index (MBI) (BI) score and Functional Independence Measure (FIM) score (P < 0.001), and obviously shorter time for completing TMT-A and TMT-B (P < 0.001). Conclusion: Performing early cognitive training combined with aerobic exercise for PSCI patients can effectively improve their QOL and promote the recovery of cognitive function. Compared with conventional health education combined with rehabilitation training, this mode presents a higher application value. Further study will be conducive to establishing a better solution for patients.

Recent Advances in Fluorescence Imaging of Traumatic Brain Injury in Animal Models.

Traumatic brain injury (TBI) is one of the top three specific neurological disorders, requiring reliable, rapid, and sensitive imaging of brain vessels, tissues, and cells for effective diagnosis and treatment. Although the use of medical imaging such as computed tomography (CT) and magnetic resonance imaging (MRI) for the TBI detection is well established, the exploration of novel TBI imaging techniques is of great interest. In this review, recent advances in fluorescence imaging for the diagnosis and evaluation of TBI are summarized and discussed in three sections: imaging of cerebral vessels, imaging of brain tissues and cells, and imaging of TBI-related biomarkers. Design strategies for probes and labels used in TBI fluorescence imaging are also described in detail to inspire broader applications. Moreover, the multimodal TBI imaging platforms combining MRI and fluorescence imaging are also briefly introduced. It is hoped that this review will promote more studies on TBI fluorescence imaging, and enable its use for clinical diagnosis as early as possible, helping TBI patients get better treatment and rehabilitation.

Rehabilitation Treatment of Motor Dysfunction Patients Based on Deep Learning Brain-Computer Interface Technology.

In recent years, brain-computer interface (BCI) is expected to solve the physiological and psychological needs of patients with motor dysfunction with great individual differences. However, the classification method based on feature extraction requires a lot of prior knowledge when extracting data features and lacks a good measurement standard, which makes the development of BCI. In particular, the development of a multi-classification brain-computer interface is facing a bottleneck. To avoid the blindness and complexity of electroencephalogram (EEG) feature extraction, the deep learning method is applied to the automatic feature extraction of EEG signals. It is necessary to design a classification model with strong robustness and high accuracy for EEG signals. Based on the research and implementation of a BCI system based on a convolutional neural network, this article aims to design a brain-computer interface system that can automatically extract features of EEG signals and classify EEG signals accurately. It can avoid the blindness and time-consuming problems caused by the machine learning method based on feature extraction of EEG data due to the lack of a large amount of prior knowledge.

Knockdown of long noncoding RNA XIST mitigates the apoptosis and inflammatory injury of microglia cells after spinal cord injury through miR-27a/Smurf1 axis.

Spinal cord injury (SCI) is a devastating neuropathological condition. Long noncoding RNA X-inactive specific transcript (XIST) is an acknowledged cancer-related gene and participates in the development of SCI. However, role of XIST in SCI remains to be well revealed. Expression of XIST, miRNA-27a-3p (miR-27a) and smad ubiquitination regulatory factor 1 (Smurf1) was detected using RT-qPCR and western blotting. Cell apoptosis and inflammatory injury were assessed by sulforhodamine B (SRB) assay, flow cytometry, western blotting and enzyme-linked immunosorbent assay. The relationship among miR-27a, XIST and Smurf1 was confirmed by dual-luciferase reporter assay, RNA immunoprecipitation and RNA pull-down assay. As a result, we observed higher level of XIST and Smurf1, but lower level of miR-27a in SCI rats and lipopolysaccharide (LPS)-induced primary microglial cells. in vitro, LPS induced SCI microglia cells as described by decreased cell viability and B cell lymphoma 2 (Bcl-2) expression, and increased cell apoptosis rate, Bax and cleaved caspase 3 levels, and tumor necrosis factor α (TNF-α) and interleukin 6 (IL-6) secretions. in vivo, a T10 laminectomy caused SCI rats as evidenced by decreased Basso-Beattie-Bresnahan Locomotor Rating Scale (BBB) score and induced expression of Bax, cleaved caspase 3, TNF-α and IL-6. However, silencing of XIST could mitigate the apoptosis and inflammatory injury in LPS-induced microglia and SCI rats. Mechanically, miR-27a interacted with XIST and Smurf1 via target binding. Either miR-27a downregulation or Smurf1 overexpression partially reversed the role of XIST deletion in LPS-treated microglial cells. Collectively, knockdown of XIST could alleviate the apoptosis and inflammatory injury of SCI models in vitro and in vivo through directly modulating miR-27a/Smurf1 axis.