The invasive brain-computer interface (BCI) is a method that involves implanting microelectrodes into brain tissue to collect neural electrical signals. The signals obtained through this method are often of high precision and relatively stable. However, the chronic fibrotic reaction resulting from long-term implantation can significantly impair the quality of the collected brain electrical signals. Therefore, ensuring the long-term stability of signal acquisition is a major challenge in the development of invasive BCI. This paper systematically reviews the formation mechanisms of fibrosis at the electrode interface, elaborating on the progression from acute inflammatory responses to the development of chronic glial scars and the formation of the extracellular matrix (ECM). It introduces the roles, advantages, and disadvantages of three anti-fibrosis strategies: material and surface optimization, drug and biological factor intervention, and integration of immune regulation and tissue engineering. This paper also evaluates their practical effects and limitations in animal and human clinical applications. Finally, it highlights the importance of establishment of standardized follow-up recording mechanisms in ensuring the long-term reliability and stability of invasive BCIs, providing references and insights for future in-depth interface optimization and clinical translation.

ObjectiveTo observe the pharmacodynamic efficacy of phlorizin in improving hepatic glycolipid metabolism disorders in type 2 diabetic mellitus （T2DM） rats and to explore its mechanism of action based on the insulin receptor substrate-1 （IRS-1）/phosphatidylinositol 3-kinase （PI3K）/protein kinase B （Akt） signaling pathway. MethodsA high-fat diet and streptozotocin （STZ） were used to establish T2DM rat models. The rats were randomly assigned into six groups： the blank control group， model group， metformin group （300 mg·kg^-1）， and phlorizin high-dose （100 mg·kg^-1） and low-dose groups （25 mg·kg^-1）. The rats were given intragastric administration for 6 weeks. The changes in body weight and fasting blood glucose （FBG） were observed， and the oral glucose tolerance test （OGTT） was carried out. The levels of total cholesterol （TC）， triglyceride （TG）， low-density lipoprotein cholesterol （LDL-C）， high-density lipoprotein cholesterol （HDL-C）， glycated serum protein （GSP）， aspartate aminotransferase （AST）， and alanine aminotransferase （ALT） in serum were detected by an automatic biochemical analyzer. The levels of fasting insulin （FINS）， interleukin （IL）-1β， IL-6， and tumour necrosis factor （TNF）-α were detected by enzyme-linked immunosorbent assay （ELISA）. The levels of superoxide dismutase （SOD） and malondialdehyde （MDA） were detected by the biochemical assays. The pancreas index， liver index， and insulin resistance index were calculated. Hematoxylin-eosin （HE） staining was used to evaluate the pathological changes in liver and pancreatic tissues. The immunofluorescence method was used to detect the changes in insulin and glucagon in pancreatic tissue. Western blot was used to detect the expression of related proteins in the IRS-1/PI3K/Akt pathway of liver tissue and its downstream glycogen synthase kinase-3β （GSK-3β） and forkhead box transcription factor O1 （FoxO1） proteins. ResultsCompared with the blank control group， the body weight of rats in the model group continued to decrease， while the FBG level increased significantly. The area under the OGTT blood glucose curve （AUC）， GSP， TC， TG， LDL-C， IL-1β， IL-6， TNF-α， MDA， pancreatic index and liver index increased significantly， while the levels of HDL-C， SOD， and FINS decreased significantly （P0.05， P0.01）. Histological results showed that the pancreatic islets of rats in the model group exhibited atrophy and severe structural abnormalities. The insulin-positive β-cells decreased significantly （P0.01）， while the glucagon-positive α-cells increased significantly （P0.01）. Inflammatory cell infiltration and partial necrosis were observed in the liver tissues of the model group rats. The expressions of p-IRS-1/IRS-1， p-GSK-3β/GSK-3β， and p-FoxO1/FoxO1 proteins in the liver of the model group increased significantly （P0.01）， while the expressions of p-PI3K/PI3K and p-Akt/Akt proteins decreased significantly （P0.01）. Compared with the model group， the diabetic symptoms of rats in all administration groups were improved. The changes in body weight and FBG were close to those of the blank control group. The levels of OGTT-AUC， GSP， TC， TG， LDL-C， MDA， IL-1β， IL-6， TNF-α and the pancreatic index， liver index were obviously reduced （P0.05， P0.01）， while the levels of HDL-C， SOD， and FINS obviously increased （P0.05， P0.01）. The pathological changes of the pancreas and liver in rats in all treatment groups were effectively improved. The insulin-positive β-cells in the pancreas increased significantly （P0.01）， while the glucagon-positive α-cells decreased significantly （P0.01）. The protein expressions of p-IRS-1/IRS-1， p-GSK-3β/GSK-3β， and p-FoxO1/FoxO1 in the liver were significantly reduced （P0.01）， while the protein expressions of p-PI3K/PI3K and p-Akt/Akt significantly increased （P0.01）. ConclusionPhlorizin reversed the weight loss and abnormal increase of FBG in T2DM rats， improved blood lipid profiles， oxidative stress， and inflammatory levels， alleviated insulin resistance， and had certain protective effects on the liver and pancreas. The hypoglycemic mechanism may involve regulating the IRS-1/PI3K/Akt signaling pathway to inhibit the activities of GSK-3β and FoxO1， thereby promoting liver glycogen synthesis and suppressing hepatic gluconeogenesis， ultimately improving glycolipid metabolism disorders.

ObjectiveTo observe the pharmacodynamic efficacy of phlorizin in improving hepatic glycolipid metabolism disorders in type 2 diabetic mellitus （T2DM） rats and to explore its mechanism of action based on the insulin receptor substrate-1 （IRS-1）/phosphatidylinositol 3-kinase （PI3K）/protein kinase B （Akt） signaling pathway. MethodsA high-fat diet and streptozotocin （STZ） were used to establish T2DM rat models. The rats were randomly assigned into six groups： the blank control group， model group， metformin group （300 mg·kg^-1）， and phlorizin high-dose （100 mg·kg^-1） and low-dose groups （25 mg·kg^-1）. The rats were given intragastric administration for 6 weeks. The changes in body weight and fasting blood glucose （FBG） were observed， and the oral glucose tolerance test （OGTT） was carried out. The levels of total cholesterol （TC）， triglyceride （TG）， low-density lipoprotein cholesterol （LDL-C）， high-density lipoprotein cholesterol （HDL-C）， glycated serum protein （GSP）， aspartate aminotransferase （AST）， and alanine aminotransferase （ALT） in serum were detected by an automatic biochemical analyzer. The levels of fasting insulin （FINS）， interleukin （IL）-1β， IL-6， and tumour necrosis factor （TNF）-α were detected by enzyme-linked immunosorbent assay （ELISA）. The levels of superoxide dismutase （SOD） and malondialdehyde （MDA） were detected by the biochemical assays. The pancreas index， liver index， and insulin resistance index were calculated. Hematoxylin-eosin （HE） staining was used to evaluate the pathological changes in liver and pancreatic tissues. The immunofluorescence method was used to detect the changes in insulin and glucagon in pancreatic tissue. Western blot was used to detect the expression of related proteins in the IRS-1/PI3K/Akt pathway of liver tissue and its downstream glycogen synthase kinase-3β （GSK-3β） and forkhead box transcription factor O1 （FoxO1） proteins. ResultsCompared with the blank control group， the body weight of rats in the model group continued to decrease， while the FBG level increased significantly. The area under the OGTT blood glucose curve （AUC）， GSP， TC， TG， LDL-C， IL-1β， IL-6， TNF-α， MDA， pancreatic index and liver index increased significantly， while the levels of HDL-C， SOD， and FINS decreased significantly （P0.05， P0.01）. Histological results showed that the pancreatic islets of rats in the model group exhibited atrophy and severe structural abnormalities. The insulin-positive β-cells decreased significantly （P0.01）， while the glucagon-positive α-cells increased significantly （P0.01）. Inflammatory cell infiltration and partial necrosis were observed in the liver tissues of the model group rats. The expressions of p-IRS-1/IRS-1， p-GSK-3β/GSK-3β， and p-FoxO1/FoxO1 proteins in the liver of the model group increased significantly （P0.01）， while the expressions of p-PI3K/PI3K and p-Akt/Akt proteins decreased significantly （P0.01）. Compared with the model group， the diabetic symptoms of rats in all administration groups were improved. The changes in body weight and FBG were close to those of the blank control group. The levels of OGTT-AUC， GSP， TC， TG， LDL-C， MDA， IL-1β， IL-6， TNF-α and the pancreatic index， liver index were obviously reduced （P0.05， P0.01）， while the levels of HDL-C， SOD， and FINS obviously increased （P0.05， P0.01）. The pathological changes of the pancreas and liver in rats in all treatment groups were effectively improved. The insulin-positive β-cells in the pancreas increased significantly （P0.01）， while the glucagon-positive α-cells decreased significantly （P0.01）. The protein expressions of p-IRS-1/IRS-1， p-GSK-3β/GSK-3β， and p-FoxO1/FoxO1 in the liver were significantly reduced （P0.01）， while the protein expressions of p-PI3K/PI3K and p-Akt/Akt significantly increased （P0.01）. ConclusionPhlorizin reversed the weight loss and abnormal increase of FBG in T2DM rats， improved blood lipid profiles， oxidative stress， and inflammatory levels， alleviated insulin resistance， and had certain protective effects on the liver and pancreas. The hypoglycemic mechanism may involve regulating the IRS-1/PI3K/Akt signaling pathway to inhibit the activities of GSK-3β and FoxO1， thereby promoting liver glycogen synthesis and suppressing hepatic gluconeogenesis， ultimately improving glycolipid metabolism disorders.

As the core vehicle for preserving and transmitting traditional Chinese medicine（TCM） academic thought and clinical experience， the establishment of a robust quality evaluation system for TCM clinical case reports is a crucial component in the current standardization and modernization of TCM. Based on the practical experience of constructing the China Clinical Cases Library of Traditional Chinese Medicine by the China Association of Chinese Medicine， this study conducted a comprehensive analysis of critical challenges， including insufficient authenticity and unfocused evaluation criteria. It proposed a three-dimensional evaluation framework grounded in the structure-process-outcome logic， encompassing three dimensions of authenticity and standardization， characteristics and advantages， application and translational impact. This framework integrated 12 key evaluation indicators in a systematic manner. The model preserved the academic characteristics of TCM syndrome differentiation and treatment， while aligning with modern scientific research standards， achieving a balance between individualized TCM experience and standardized evaluation. Concurrently， this study provided theoretical foundations and methodological guidance for evaluating the quality of TCM clinical cases， contributing significantly to the inheritance of TCM knowledge， evidence-based practice， and the reform of talent evaluation mechanisms.

Objective To systematically evaluate the efficacy and safety of video-assisted thoracoscopic surgery (VATS) with different numbers of ports in the treatment of spontaneous pneumothorax. Methods We conducted a comprehensive search of CNKI, PubMed, The Cochrane Library, Web of Science, EMbase, Wanfang Data, and the Chinese Medical Journal Full-text Database for clinical controlled trials on VATS with different port numbers for spontaneous pneumothorax, from their inception to March 2023. Two researchers independently screened the literature and assessed its quality.The Newcastle-Ottawa Scale (NOS) was used to assess the methodological quality of cohort and case-control studies, and the Cochrane risk-of-bias tool was used to evaluate randomized controlled trials (RCT). Meta-analysis was performed using RevMan 5.4.1 software. Results A total of 107 studies were included, comprising 35 RCT, 2 cohort studies, and 70 case-control studies. All cohort and case-control studies included in the analysis had NOS scores≥7. The meta-analysis revealed that compared to two-port VATS (2P-VATS) and three-port VATS (3P-VATS), single-port thoracoscopic surgery (SPTS) was associated with less intraoperative blood loss (SMD=–1.58, 95%CI: –1.93 to –1.22, P<0.001; and SMD=–1.59, 95%CI: –2.03 to –1.14, P<0.001, respectively), shorter postoperative hospital stay (SMD=–1.05, 95%CI: –1.29 to –0.82, P<0.001; and SMD=–1.08, 95%CI: –1.39 to –0.77, P<0.001), shorter duration of postoperative chest tube drainage (SMD=–0.75, 95%CI: –1.00 to –0.50, P<0.001; and SMD=–1.23, 95%CI: –1.72 to –0.75, P<0.001), fewer postoperative complications (OR=0.34, 95%CI: 0.26 to 0.45, P<0.001; and OR=0.47, 95%CI: 0.33 to 0.68, P<0.001), and lower pain scores at 24, 48, and 72 hours after surgery (P<0.05). The operative time for SPTS was shorter than that for 2P-VATS (SMD=–0.53, 95%CI: –0.90 to –0.16, P=0.005) but showed no significant difference compared to 3P-VATS (P=0.21). When comparing 2P-VATS with 3P-VATS, 2P-VATS demonstrated less intraoperative blood loss (SMD=–1.02, 95%CI: –1.81 to –0.22, P=0.01), shorter postoperative hospital stay (SMD=–0.59, 95%CI: –1.11 to –0.06, P=0.03), shorter duration of chest tube drainage (SMD=–0.46, 95%CI: –0.85 to –0.08, P=0.02), fewer postoperative complications (OR=0.36, 95%CI: 0.22 to 0.59, P<0.001), and lower pain scores at 24, 48, and 72 hours after surgery (P≤0.05). Conclusion Both SPTS and 2P-VATS are effective and safe surgical options for spontaneous pneumothorax, deserving further promotion and application in clinical practice. However, due to limitations in the quantity and quality of the included studies, more large-sample, high-quality research is needed to validate these findings.

Objective To investigate the imaging characteristics of patients with cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy （CADASIL）carrying cysteine-altering versus non-cysteine-altering NOTCH3 mutations. Methods A retrospective analysis was performed for 19 patients with CADASIL who attended Department of Neurology，The Affiliated Hospital of Guizhou Medical University， among whom there were 16 patients with cysteine-altering mutations and 3 with non-cysteine-altering mutations， and PubMed database was searched to obtain 192 cases （158 patients with cysteine-altering mutations and 34 with non-cysteine-altering mutations）. The impact of these two types of mutations on lesion distribution in the temporal pole and external capsule was analyzed. Results The cysteine-altering mutation group had a significantly higher risk of temporal pole lesions compared with the non-cysteine-altering mutation group （OR=2.99，95%CI 1.37‒6.51，P=0.006）， and there was no significant difference in external capsule lesions between the two groups （OR=2.31，95%CI 0.75‒6.48，P=0.12）. External capsule lesions were associated with age （OR=1.04，95%CI 1.01‒1.07， P=0.02）.Sex showed no significant influence on lesion distribution（OR=1.72，95%CI 0.67‒4.67，P=0.27；temporal pole：OR=0.54，95%CI 0.27‒1.05， P=0.07）. Conclusion Cysteine-altering NOTCH3 mutations are an independent risk factor for temporal pole lesions，while external capsule lesions are closely associated with age. This suggests that temporal pole lesions might be a specific imaging marker for cysteine-altering mutations， whereas external capsule lesions can reflect age-related disease progression.

Mitofusin 2 (MFN2) residing on the outer mitochondrial membrane is a pivotal factor participating in mitochondrial fusion and maintaining mitochondrial morphology. Due to its multifaceted cellular functions, MFN2 is implicated in the pathogenesis of diverse maladies, notably type 2 Charcot-Marie-Tooth disease, which has catalyzed a surge in pharmaceutical endeavors directed towards MFN2. This article reviews the function of MFN2 and its role in a variety of diseases, outlines the current status of drug discovery against MFN2, and summarizes potential drug molecules currently in preclinical research, aiming to provide some reference for the research and development of drugs and therapies targeting MFN2.

Objective To analyze the characteristics and causes of an occupational acute carbon monoxide poisoning incident caused by a nitrogen generator malfunction. Methods The workers and the workshop from an electronic component manufacturing company in Guangzhou City, which had an occupational acute carbon monoxide poisoning incident, were selected as the research subjects using the retrospective investigation method. Relevant data of worksite survey of occupational health, clinical records of poisoning patients, and occupational disease diagnosis data were collected for analysis. Results A total of 15 workers who experienced discomfort in this incident, were from the final inspection workshop using high-purity nitrogen (purity of 99.999%). The short-term exposure concentration of carbon monoxide in the workplace air at three oven operating posts using high-purity nitrogen was 64.1, 581.0, and 142.0 mg/m³, respectively, while the concentration in the workplace air at the oven operating posts using regular nitrogen and the nitrogen-generating room was <0.1 mg/m³. Carboxyhemoglobin saturation levels in the 15 patients ranged from 2.000%-17.300%. Occupational acute mild carbon monoxide poisoning was diagnosed in nine patients, occupational acute carbon monoxide exposure reactions was diagnosed in six patients. This poisoning incident was caused by machine malfunction and improper operation, leading to occupational acute carbon monoxide poisoning. Conclusion Companies using nitrogen production machine should enhance their ability to identify carbon monoxide risks, strengthen training and management of workers, establish emergency response plans for nitrogen production and use, ensure proper maintenance of production equipment, and optimize operational procedures to prevent acute poisoning incidents.

To understand the progress of, summarize the lessons learned from and analyze the challenges in the national schistosomiasis elimination program of China in 2024, this article presented the endemic situation of schistosomiasis and national schistosomiasis surveillance results in the People’s Republic of China in 2024. By the end of 2024, Shanghai Municipality, Zhejiang Province, Fujian Province, Guangdong Province and Guangxi Zhuang Autonomous Region continued to consolidate schistosomiasis elimination achievements, and 7 provinces of Jiangsu, Sichuan, Yunnan, Hubei, Hunan, Anhui and Jiangxi maintained the criteria of schistosomiasis transmission interruption. A total of 450 counties (cites, districts) were found to be endemic for schistosomiasis in China in 2024, including 26 061 endemic villages covering 73 630 500 residents at risk of infections. Among the 450 counties (cities, districts) endemic for schistosomiasis, 388 (86.22%) achieved the criteria of schistosomiasis elimination and 62 (13.78%) achieved the criteria of transmission interruption. In 2024, a total of 4 102 624 individuals received immunological tests for schistosomiasis in China, with 44 823 sero-positives identified (1.09% seroprevalence), and a total of 169 722 individuals received parasitological examinations, with 1 egg-positives detected. A total of 27 321 cases with advanced schistosomiasis were documented in China by the end of 2024. In 2024, a total of 575 686 bovines were raised in schistosomiasis-endemic villages of China, and 113 842 bovines received immunological tests, with 235 sero-positives detected (0.21% seroprevalence), while no egg-positives were identified among the 167 475 bovines receiving parasitological examinations. In 2024, snail survey was performed covering an area of 680 498.27 hm² in China, and 190 778.66 hm² snail habitats were identified, including 59.09 hm² emerging snail habitats and 704.23 hm² reemerging snail habitats. In 2024, a total of 19 665 schistosomiasis patients receiving chemotherapy with praziquantel in China, and expanded chemotherapy was given to humans at 571 722 person-times and to bovines at 306 740 herd-times. In addition, snail control with chemical treatment covered 117 111.37 hm² snail habitats across China in 2024, and the actual area of chemical treatment was 66 562.95 hm², while environmental improvements were performed in snail habitats covering an area of 1 374.26 hm². The national schistosomiasis surveillance results showed that the mean prevalence rates of Schistosoma japonicum infections were both 0 among humans and bovines in China in 2024, and no S. japonicum infection was detected in snails. These data demonstrated that the prevalence of schistosomiasis remained at a low level in China in 2024; however, the areas of snail habitats remained high and the number of fenced cattle showed a slight increase. To address these risks, it is imperative to maintain the integrated strategy with an emphasis on management of the source of S. japonicum infection and intensified snail control in high-risk areas, and to reinforce schistosomiasis surveillance and forecast and snail control in high-risk areas.

Malaria, a parasitic disease caused by infection with the species of Plasmodium and transmitted by Anopheles mosquito bites, is one of the major public health challenges that seriously threaten human health. Malaria parasites present diverse immune escape strategies to escape from the recognition and clearance of the host immune system, which poses a great challenge to the malaria control programme. This review presents the advances in the mechanisms underlying the immune escape of Plasmodium, including antigenic variation, epigenetic regulation, antagonism against IgM antibody, activation of the cyclic guanosine monophosphate-adenosine monophosphate (GMP-AMP) synthase-stimulator of interferon genes (cGAS-STING) signaling, suppression of splenic immune functions, and molecular camouflage, so as to provide insights into development of malaria vaccines and antimalarial agents and formulation of the malaria control strategy.