Repetitive transcranial magnetic stimulation for chemotherapy-induced peripheral neuropathy in multiple myeloma: A pilot study.

Objective: Chemotherapy-induced peripheral neuropathy is one of the major toxicities in multiple myeloma patients, often resulting in dose reductions or treatment interruptions. Repetitive transcranial magnetic stimulation is a safe non-invasive neuromodulation therapy with potential benefits for chemotherapy-induced peripheral neuropathy. The objective of this study was to investigate the efficacy of repetitive transcranial magnetic stimulation treatment on chemotherapy-induced peripheral neuropathy in multiple myeloma patients. Materials and methods: We screened 30 multiple myeloma patients with chemotherapy-induced peripheral neuropathy who underwent repetitive transcranial magnetic stimulation treatment in this study. Prior to and following repetitive transcranial magnetic stimulation treatment, patients were assessed with nerve conduction velocity, visual analog scale and the European Organization of Research and Treatment of Cancer Quality of Life Questionnaire-CIPN 20-item scale (EORTC QLQ-CIPN20). Categorical and continuous variables were analyzed using Fisher's exact test and Mann-Whitney U test respectively. A p-value < 0.05 (2-tailed) was considered statistically significant. Results: Following repetitive transcranial magnetic stimulation treatment, 24/30 (80.0%) patients reported a reduction in chemotherapy-induced peripheral neuropathy symptoms. Meanwhile, all 15 patients with grade 2 chemotherapy-induced peripheral neuropathy experienced improvements about themselves, compared to 8/10 patient with grade 3 chemotherapy-induced peripheral neuropathy and 1/5 with grade 4 chemotherapy-induced peripheral neuropathy. Visual analog scale scores decreased after repetitive transcranial magnetic stimulation treatment (5.40 ± 1.94 vs 3.10 ± 1.60, p < 0.001). We also observed enhancements in both motor conduction velocity and sensory conduction velocity of patients in bilateral median nerves, posterior tibial nerves, common ulnar nerves and peroneal nerves following repetitive transcranial magnetic stimulation treatment. Analysis of the European Organization of Research and Treatment of Cancer Quality of Life Questionnaire-CIPN 20-item scale data (17.68 ± 8.14 vs 10.50 ± 9.55, p < 0.001) revealed significant reductions in scores. Patients with grade 2-3 (n = 25) exhibited a mean reduction of 8.89 ± 4.24 points, while those with grade 4 (n = 5) showed a difference value of 3.54 ± 3.45, p < 0.001. No adverse events were observed. Conclusion: Our findings suggest that repetitive transcranial magnetic stimulation is a safe and effective therapeutic approach for ameliorating peripheral nerve injury and alleviating the chemotherapy-induced peripheral neuropathy symptoms in multiple myeloma patients. Early initiation of repetitive transcranial magnetic stimulation treatment may yield more favorable outcomes for these patients.

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.

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.