Neurological disorders such as post-stroke hemiplegia, spinal cord injury, and Parkinson disease represent a major global health burden. Brain-computer interface (BCI), which creates direct communication pathways between the nervous system and external devices, offers a promising strategy for functional restoration. The long-term efficacy of such BCI fundamentally depends on the performance of biomaterials at the neural interface. Ideal materials must concurrently satisfy biocompatibility, electrical conductivity, enduring chemical stability, and mechanical compatibility with brain tissue. This review systematically outlines the application of conductive polymers, inorganic nanomaterials, natural biomaterials, and composites in BCI, with a focus on how advanced designs, such as bionic and encapsulated electrodes, improve signal fidelity and surgical feasibility through structural innovation. It further summarizes key material-modification techniques and analyzes the complex foreign-body response orchestrated by microglia, astrocytes, and peripheral immune cells. Finally, it provides insights into future research directions and clinical translation of BCI-based neurorehabilitation, while highlighting critical challenges including long-term biosafety and the establishment of standardized evaluation frameworks, aiming to bridge the gap between laboratory innovation and effective clinical deployment.

Neurofibromas are benign peripheral nerve sheath tumors. It is more common in neurofibromatosis type Ⅰ. However, isolated vagal nerve neurofibroma（VNN） of the neck is extremely rare, and only a few case reports have been reported. Its etiology and pathogenesis are not clear. The diagnosis is mainly based on pathological examination and immunohistochemistry, and surgical resection is the main treatment. This study reports a rare case of giant solitary vagus neurofibroma in the neck. The patient was a 29-year-old female who was found to have a mass on the right side of the neck by physical examination, which was considered to be a vagus nerve tumor by neck ultrasound and imaging examination. The tumor was completely removed during the operation, with the size of about 10.0 cm×2.5 cm, and the patient had no special discomfort. Postoperative pathology and immunohistochemistry confirmed neurofibroma. After surgery, the patient had right vocal cord paralysis, hoarseness, choking and paroxysmal cough. After swallowing function training and voice rehabilitation treatment in the department, the patient recovered satisfactorily. There was no complication and recurrence during the follow-up of 1 year. This article reviews the literature to improve the diagnosis and treatment of solitary vagus neurofibroma in the neck by combining its medical history, imaging features, pathology and immunohistochemistry, and surgical treatment.
Humans ; Female ; Adult ; Neurofibroma ; Vagus Nerve/pathology* ; Neck ; Cranial Nerve Neoplasms

Lung adenocarcinoma (LUAD) is a global malignancy with significant chemoresistance impacting patient prognosis. The pro-tumorigenic role of hyaluronan-mediated motility receptor (HMMR) in LUAD is recognized. This study was designed to investigate the underlying mechanisms by which HMMR affects chemoresistance in LUAD. Bioinformatics presented the expression patterns of HMMR in LUAD patients and the association between HMMR levels and patient survival, followed by qRT-PCR to verify HMMR expression in LUAD tissues and cells. Further, bioinformatics was leveraged to identify the signaling pathways enriched by HMMR and its relevance to glycolytic genes, we also analyzed changes in the glycolytic activity of LUAD cells by manipulating HMMR expression. Stemness was evaluated through cell aggregation assays and Western blot, and drug responsiveness was gauged using CCK-8 assays, alongside flow cytometry for apoptosis analysis. HMMR was highly expressed in LUAD tissues and cells, and this overexpression correlated with poorer prognoses in patients. GSEA showed that HMMR was notably enriched in the glycolysis and gluconeogenesis pathways, correlating positively with the expression of key glycolytic genes. Cellular experiments confirmed that HMMR knockdown notably suppressed aerobic glycolysis in LUAD cells. Moreover, overexpression of HMMR could further enhance the stemness and cisplatin resistance of LUAD cells by stimulating glycolysis. In brief, this study has validated that high levels of HMMR in LUAD are predictive of poor patient prognosis, and that overexpression of HMMR can catalyze aerobic glycolysis, thus promoting stemness and chemoresistance in LUAD cells. Thus, HMMR could be a target for improving chemosensitivity in LUAD.

Lung adenocarcinoma (LUAD) is a global malignancy with significant chemoresistance impacting patient prognosis. The pro-tumorigenic role of hyaluronan-mediated motility receptor (HMMR) in LUAD is recognized. This study was designed to investigate the underlying mechanisms by which HMMR affects chemoresistance in LUAD. Bioinformatics presented the expression patterns of HMMR in LUAD patients and the association between HMMR levels and patient survival, followed by qRT-PCR to verify HMMR expression in LUAD tissues and cells. Further, bioinformatics was leveraged to identify the signaling pathways enriched by HMMR and its relevance to glycolytic genes, we also analyzed changes in the glycolytic activity of LUAD cells by manipulating HMMR expression. Stemness was evaluated through cell aggregation assays and Western blot, and drug responsiveness was gauged using CCK-8 assays, alongside flow cytometry for apoptosis analysis. HMMR was highly expressed in LUAD tissues and cells, and this overexpression correlated with poorer prognoses in patients. GSEA showed that HMMR was notably enriched in the glycolysis and gluconeogenesis pathways, correlating positively with the expression of key glycolytic genes. Cellular experiments confirmed that HMMR knockdown notably suppressed aerobic glycolysis in LUAD cells. Moreover, overexpression of HMMR could further enhance the stemness and cisplatin resistance of LUAD cells by stimulating glycolysis. In brief, this study has validated that high levels of HMMR in LUAD are predictive of poor patient prognosis, and that overexpression of HMMR can catalyze aerobic glycolysis, thus promoting stemness and chemoresistance in LUAD cells. Thus, HMMR could be a target for improving chemosensitivity in LUAD.

Lung adenocarcinoma (LUAD) is a global malignancy with significant chemoresistance impacting patient prognosis. The pro-tumorigenic role of hyaluronan-mediated motility receptor (HMMR) in LUAD is recognized. This study was designed to investigate the underlying mechanisms by which HMMR affects chemoresistance in LUAD. Bioinformatics presented the expression patterns of HMMR in LUAD patients and the association between HMMR levels and patient survival, followed by qRT-PCR to verify HMMR expression in LUAD tissues and cells. Further, bioinformatics was leveraged to identify the signaling pathways enriched by HMMR and its relevance to glycolytic genes, we also analyzed changes in the glycolytic activity of LUAD cells by manipulating HMMR expression. Stemness was evaluated through cell aggregation assays and Western blot, and drug responsiveness was gauged using CCK-8 assays, alongside flow cytometry for apoptosis analysis. HMMR was highly expressed in LUAD tissues and cells, and this overexpression correlated with poorer prognoses in patients. GSEA showed that HMMR was notably enriched in the glycolysis and gluconeogenesis pathways, correlating positively with the expression of key glycolytic genes. Cellular experiments confirmed that HMMR knockdown notably suppressed aerobic glycolysis in LUAD cells. Moreover, overexpression of HMMR could further enhance the stemness and cisplatin resistance of LUAD cells by stimulating glycolysis. In brief, this study has validated that high levels of HMMR in LUAD are predictive of poor patient prognosis, and that overexpression of HMMR can catalyze aerobic glycolysis, thus promoting stemness and chemoresistance in LUAD cells. Thus, HMMR could be a target for improving chemosensitivity in LUAD.

Lung adenocarcinoma (LUAD) is a global malignancy with significant chemoresistance impacting patient prognosis. The pro-tumorigenic role of hyaluronan-mediated motility receptor (HMMR) in LUAD is recognized. This study was designed to investigate the underlying mechanisms by which HMMR affects chemoresistance in LUAD. Bioinformatics presented the expression patterns of HMMR in LUAD patients and the association between HMMR levels and patient survival, followed by qRT-PCR to verify HMMR expression in LUAD tissues and cells. Further, bioinformatics was leveraged to identify the signaling pathways enriched by HMMR and its relevance to glycolytic genes, we also analyzed changes in the glycolytic activity of LUAD cells by manipulating HMMR expression. Stemness was evaluated through cell aggregation assays and Western blot, and drug responsiveness was gauged using CCK-8 assays, alongside flow cytometry for apoptosis analysis. HMMR was highly expressed in LUAD tissues and cells, and this overexpression correlated with poorer prognoses in patients. GSEA showed that HMMR was notably enriched in the glycolysis and gluconeogenesis pathways, correlating positively with the expression of key glycolytic genes. Cellular experiments confirmed that HMMR knockdown notably suppressed aerobic glycolysis in LUAD cells. Moreover, overexpression of HMMR could further enhance the stemness and cisplatin resistance of LUAD cells by stimulating glycolysis. In brief, this study has validated that high levels of HMMR in LUAD are predictive of poor patient prognosis, and that overexpression of HMMR can catalyze aerobic glycolysis, thus promoting stemness and chemoresistance in LUAD cells. Thus, HMMR could be a target for improving chemosensitivity in LUAD.

Lung adenocarcinoma (LUAD) is a global malignancy with significant chemoresistance impacting patient prognosis. The pro-tumorigenic role of hyaluronan-mediated motility receptor (HMMR) in LUAD is recognized. This study was designed to investigate the underlying mechanisms by which HMMR affects chemoresistance in LUAD. Bioinformatics presented the expression patterns of HMMR in LUAD patients and the association between HMMR levels and patient survival, followed by qRT-PCR to verify HMMR expression in LUAD tissues and cells. Further, bioinformatics was leveraged to identify the signaling pathways enriched by HMMR and its relevance to glycolytic genes, we also analyzed changes in the glycolytic activity of LUAD cells by manipulating HMMR expression. Stemness was evaluated through cell aggregation assays and Western blot, and drug responsiveness was gauged using CCK-8 assays, alongside flow cytometry for apoptosis analysis. HMMR was highly expressed in LUAD tissues and cells, and this overexpression correlated with poorer prognoses in patients. GSEA showed that HMMR was notably enriched in the glycolysis and gluconeogenesis pathways, correlating positively with the expression of key glycolytic genes. Cellular experiments confirmed that HMMR knockdown notably suppressed aerobic glycolysis in LUAD cells. Moreover, overexpression of HMMR could further enhance the stemness and cisplatin resistance of LUAD cells by stimulating glycolysis. In brief, this study has validated that high levels of HMMR in LUAD are predictive of poor patient prognosis, and that overexpression of HMMR can catalyze aerobic glycolysis, thus promoting stemness and chemoresistance in LUAD cells. Thus, HMMR could be a target for improving chemosensitivity in LUAD.

Objective The aim of this study was to explore the effectiveness of self-made oral humidity detection device to assist in evaluating the degree of parotid gland damage in radiotherapy for nasopharyngeal carcinoma,so as to guide doctors to change the radiotherapy plan in time,reduce the radiation dose to parotid gland,and reduce the incidence of xerostomia after radiotherapy.Methods A retrospective analysis was conducted on the relationship between oral humidity and parotid gland dose of radiotherapy in 60 patients with nasopharyngeal carcinoma using oral detection devices in the Department of Oncology of Southwest Medical University Affiliated Hospital from January 1,2022 to December 31,2022.According to the method of changing the radiotherapy plan,patients were divided into experimental group(n=30)and control group(n=30).The patients in the experimental group used a self-made oral humidity detection device to detect oral humidity,when 30 patients with oral relative humidity below 65%underwent CT simulation positioning and changed the radiotherapy plan to reduce the dose of parotid gland;The control group patients collected oral humidity but did not interfere in the radiotherapy plan,and only underwent CT positioning during the mid-term radiotherapy.The average oral humidity,parotid gland,and target area dose parameters of patients were analyzed after radiotherapy.The follow-up questionnaire was conducted to evaluate the life quality of patients in terms of dry mouth,decreased taste,difficulty opening mouth,and dental caries in two groups.Results The average oral humidity(t=2.938,P<0.05),the Dmean of average dose of bilateral parotid glands(tleft=-2.076,tright=-2.094,P<0.05),the D50 for dose of 50%volume of bilateral parotid glands(tleft=-2.123,tright=-2.230,P<0.05),and the volume percentage V30 of bilateral parotid gland dose(tleft=-2.505,tright=-2.491,P<0.05)in patients were significantly re-duced in the experimental group compared to the control group,while there was no statistically significant differences in target area do-simetric parameters(P>0.05).The dry mouth and taste loss in the experimental group were lower than those of the control group(P<0.05),and the difficulty in opening the mouth and caries scores were lower than those of the control group,but the difference was not statistically significant(P>0.05).Conclusion The oral humidity detection device can detect the oral humidity of radiotherapy pa-tients in time,objectively evaluate the impact of radiation on patient's parotid gland,guide doctors to change the radiotherapy treatment plan in a timely manner,minimize the degree of parotid gland damage,and improve their quality of life in nasopharyngeal carcinoma radiotherapy patients.At the same time,the device is easy to operate,time-consuming,and non-invasive,which improves the effec-tiveness and safety of radiotherapy technology and is worth promoting this device.

Objective To explore the establishment of a subcutaneously transplanted tumor model of hepatocellular carcinoma in mice with Qi stagnation and blood stasis syndrome.Methods Forty male C57BL/6 mice were randomly divided into 4 groups:NC group,QZXY group,Tumor group,and QZXY+Tumor group.They were categorized based on the modeling of Qi stagnation and blood stasis syndrome(7 days)combined with the modeling of subcutaneous transplantation of hepatocellular carcinoma tumor(20 days).Observations were conducted of the syndrome manifestations as well as the tumor size and weight of the mice after modeling.Results(1)Body weight:on the 7th day of modeling,the weights of the QZXY group and QZXY+Tumor group were significantly lower than that of the NC group(P＜0.05).(2)Body temperature:on the 7th day of modeling,body temperature significantly decreased in the QZXY group(P＜0.05),while it increased in the Tumor group(P＜0.05)compared with the NC group.On the 27th day of modeling,the temperature of the QZXY+Tumor group was significantly lower than that of the NC group(P＜0.05).(3)Syndrome manifestations:according to the syndrome scoring table,mice in both the QZXY group and QZXY+Tumor group exhibited Qi stagnation and blood stasis syndrome on the 7th day of modeling(P＜0.05).As modeling time extended,the score of mice in the Tumor group increased with the formation of the tumor,and the score of mice in the QZXY+Tumor group was significantly higher than that of the other three groups(P＜0.05).(4)Claw petechiae:the number of claw petechiae significantly increased in all three groups of modeled mice compared with the NC group(P＜0.05),with the QZXY+Tumor group showing the highest number.(5)Claw r value:the r value of the claw was significantly lower in all three groups of modeled mice than that in the NC group(P＜0.05).Additionally,the r value of the claw in the QZXY+Tumor group was consistently lower than that of the other three groups.(6)Open field activity:the vertical and horizontal activity of mice in the QZXY+Tumor group decreased significantly compared with that of the NC group(P＜0.05).(7)Coagulation indexes:APTT,TT,and FIB were significantly increased in the QZXY+Tumor group(P＜0.05 or P＜0.01)compared with those in the NC group.(8)Tumor size and weight:compared with the Tumor group,the QZXY+Tumor group showed significantly increased tumor size and weight(P＜0.05).Conclusions This study successfully established a subcutaneous transplanted tumor model of hepatocellular carcinoma in mice with Qi stagnation and blood stasis syndrome.The findings indicated that Qi stagnation and blood statsis syndrome may occur during the course of live cancer.Besides,the causes inducing the Qi stagnation and blood stasis syndrome will further accelerate the progression of liver cancer.

Objective To explore the establishment of a subcutaneously transplanted tumor model of hepatocellular carcinoma in mice with Qi stagnation and blood stasis syndrome.Methods Forty male C57BL/6 mice were randomly divided into 4 groups:NC group,QZXY group,Tumor group,and QZXY+Tumor group.They were categorized based on the modeling of Qi stagnation and blood stasis syndrome(7 days)combined with the modeling of subcutaneous transplantation of hepatocellular carcinoma tumor(20 days).Observations were conducted of the syndrome manifestations as well as the tumor size and weight of the mice after modeling.Results(1)Body weight:on the 7th day of modeling,the weights of the QZXY group and QZXY+Tumor group were significantly lower than that of the NC group(P＜0.05).(2)Body temperature:on the 7th day of modeling,body temperature significantly decreased in the QZXY group(P＜0.05),while it increased in the Tumor group(P＜0.05)compared with the NC group.On the 27th day of modeling,the temperature of the QZXY+Tumor group was significantly lower than that of the NC group(P＜0.05).(3)Syndrome manifestations:according to the syndrome scoring table,mice in both the QZXY group and QZXY+Tumor group exhibited Qi stagnation and blood stasis syndrome on the 7th day of modeling(P＜0.05).As modeling time extended,the score of mice in the Tumor group increased with the formation of the tumor,and the score of mice in the QZXY+Tumor group was significantly higher than that of the other three groups(P＜0.05).(4)Claw petechiae:the number of claw petechiae significantly increased in all three groups of modeled mice compared with the NC group(P＜0.05),with the QZXY+Tumor group showing the highest number.(5)Claw r value:the r value of the claw was significantly lower in all three groups of modeled mice than that in the NC group(P＜0.05).Additionally,the r value of the claw in the QZXY+Tumor group was consistently lower than that of the other three groups.(6)Open field activity:the vertical and horizontal activity of mice in the QZXY+Tumor group decreased significantly compared with that of the NC group(P＜0.05).(7)Coagulation indexes:APTT,TT,and FIB were significantly increased in the QZXY+Tumor group(P＜0.05 or P＜0.01)compared with those in the NC group.(8)Tumor size and weight:compared with the Tumor group,the QZXY+Tumor group showed significantly increased tumor size and weight(P＜0.05).Conclusions This study successfully established a subcutaneous transplanted tumor model of hepatocellular carcinoma in mice with Qi stagnation and blood stasis syndrome.The findings indicated that Qi stagnation and blood statsis syndrome may occur during the course of live cancer.Besides,the causes inducing the Qi stagnation and blood stasis syndrome will further accelerate the progression of liver cancer.