Neurological diseases have high morbidity and disability rates， posing a severe threat to human health. Cli nical manifestations include motor， sensory， cognitive and conscious disorders. Chaihu jia longgu muli decoction is derived from Treatise on Febrile Diseases ， with the effects of harmonizing Shaoyang， activating Yang and clearing heat， and tranquilizing the mind. This paper systematically reviews the research progress in clinical application and mechanism of Chaihu jia longgu muli decoction in the field of neurological diseases. It has been found that the decoction shows favorable efficacy in various neurological diseases such as insomnia， depression， epilepsy， vertigo， migraine and vascular dementia. The specific mechanisms are related to regulating neurotransmitter levels， repairing neuronal function， alleviating neuroinflammation， improving mitochondrial dysfunction and regulating intestinal flora. In the future， standardized prospective follow-up cohorts should be established， and core outcome indicators should be clearly defined to strengthen the evidence base. Furthermore， multidisciplinary research should be leveraged to expand the therapeutic value of Chaihu jia longgu muli decoction in the management of neurological diseases.

Objective: To screen the risk factors of cesarean scar diverticula ( CSD) after cesarean section and to construct a risk prediction model． Methods: 491 cases of mothers who underwent cesarean section were recruited as the study subjects，and the data from the database of negative ultrasound of mothers who returned to the hospital 12 months after operation were collected，and the dataset was randomly divided into the training set and the test group according to 7 ∶ 3 ; the variables were screened to obtain the risk factors of CSD and the risk prediction model was constructed by the use of least absolute shrinkage and selection operator (LASSO) ; the variables were screened using the LASSO to obtain the characteristic variables，and the characteristic variables were analyzed by multifacto- rial logistic regression analysis，and the nomogram prediction model was constructed by using the R software． Results: A total of 491 cases of sample data were included，including 344 cases in the training set and 147 cases in the test set ; feature variables were screened by LASSO，and ten－fold cross－validation was used．Five variables were finally screened : number of cesarean deliveries，number of years between two cesarean deliveries，24-hour hemorrhage，operation time and uterine position(P＜0. 05) ．The accuracy of the decision analysis curves for inter- nal evaluation and internal validation of the CSD risk prediction model constructed using it was high ; the AUC (95% CI) of the diagnostic model in the training set and the test set were 0. 75 (0. 71－0. 80) and 0. 79 (0. 71 - 0. 87) ，respectively． Conclusion The risk prediction model established using the LASSO cross-validation algo- rithm has good predictive value for the occurrence of postpartum scar diverticula，which deserves clinical attention．

The management of chronic wounds presents significant challenges, characterized by a low rate of healing and substantial impairment of patients’ quality of life, while also exerting a considerable strain on healthcare resources. Wound healing is a multifactorial and dynamic process, necessitating close monitoring of wound changes and timely, appropriate interventions. Smart bandage/dressing, an innovative approach born from interdisciplinary research, offers a new generation of wound care. It enables dynamic quantitative monitoring of wound conditions; facilitates transdermal drug release and physical mode therapeutics; and adjusts interventions in real time based on monitoring outcomes. In comparison to traditional wound dressings, smart bandages exhibit attributes such as real-time responsiveness, precision, and convenience. They not only simplify wound management but also enhance patient comfort and compliance, showcasing potential as a safe and effective treatment modality. Smart bandages hold promise for elevating the efficiency of managing chronic wounds, reducing morbidity rates, alleviating the burden of disease, and ultimately improving patients’ quality of life. This paper summarized the recent research progress of smart bandages and provided insights into novel wound care strategies.

Ferroptosis has been shown to mediate the development of fibrosis.Polyphyllin Ⅶ(PP7),a bioactive component of Paris polyphylla,exhibits potent anti-inflammatory activity and can significantly alleviate liver fibrosis.In this study,treatment with PP7 significantly inhibited the proliferation and activation of hepatic stellate cells(HSCs),which could be suppressed by a ferroptosis inhibitor.In addition,it promoted HSC ferroptosis by suppressing glutathione(GSH)peroxidase 4(GPX4)and enhanced the expression of CX3C chemokine ligand 1(CX3CL1).Depletion of CX3CL1 attenuated the effects of PP7 on the activation and ferroptosis of HSCs and the expression of GPX4.Notably,CX3CL1 directly interacted with GPX4,triggering HSC ferroptosis.The transcription factor hypermethylated in cancer 1(Hic1),which binds to the Cx3cl1 promoter,increased the expression of CX3CL1.Its absence resulted in downregulation of CX3CL1,sup-pressing the GPX4-dependent ferroptosis of PP7-treated HSCs and promoting their activation.HIC1 was found to directly interact with PP7 at the GLY164 site.Co-culture experiments showed that PP7-induced HSC ferroptosis attenuated macrophage recruitment by regulating inflammation-related genes.HSC-specific inhibition of HIC1 counteracted PP7-induced collagen depletion and HSC ferroptosis in vivo.These findings suggest that PP7 induces HSC ferroptosis through the HIC1/CX3CL1/GPX4 axis.

Peri-implant diseases are characterized by the resorption of hard tissue and the inflammation of soft tissue. Epigenetics refers to alterations in the expression of genes that are not encoded in the DNA sequence, influencing diverse physiological activities, including immune response, inflammation, and bone metabolism. Epigenetic modifications can lead to tissue-specific gene expression variations among individuals and may initiate or exacerbate inflammation and disease predisposition. However, the impact of these factors on peri-implantitis remains inconclusive. To address this gap, we conducted a comprehensive review to investigate the associations between epigenetic mechanisms and peri-implantitis, specifically focusing on DNA methylation and microRNAs (miRNAs or miRs). We searched for relevant literature on PubMed, Web of Science, Scopus, and Google Scholar with keywords including "epigenetics," "peri-implantitis," "DNA methylation," and "microRNA." DNA methylation and miRNAs present a dynamic epigenetic mechanism operating around implants. Epigenetic modifications of genes related to inflammation and osteogenesis provide a new perspective for understanding how local and environmental factors influence the pathogenesis of peri-implantitis. In addition, we assessed the potential application of DNA methylation and miRNAs in the prevention, diagnosis, and treatment of peri-implantitis, aiming to provide a foundation for future studies to explore potential therapeutic targets and develop more effective management strategies for this condition. These findings also have broader implications for understanding the pathogenesis of other inflammation-related oral diseases like periodontitis.
Peri-Implantitis/genetics* ; Humans ; Epigenesis, Genetic ; DNA Methylation ; MicroRNAs/genetics*

Objective To investigate the effect of four traditional Chinese drugs for reinforcing kidney combined with Tongqiao Huoxue Decoction on serum neurotransmitters and neurological func-tion in patients with post-stroke cognitive impairment(PSCI).Methods A total of 110 patients with PSCI were randomly divided into treatment group and control group,with 55 cases in each group.The control group was treated with donepezil tablet,while the treatment group was treated with four tradi-tional Chinese drugs for reinforcing kidney and Tongqiao Huoxue Decoction on the basis of the control group.The total effective rate,the Mini-Mental State Examination(MMSE)score,the Montreal Cogni-tive Assessment(MoCA)score,the National Institutes of Health Stroke Scale(NIHSS)score and the Barthel Index(BI)as well as serum levels of acetylcholine(ACh),dopamine(DA),norepinephrine(NE),5-hydroxytryptamine(5-HT),neuron-specific enolase(NSE),visinin-like protein-1(VILIP-1),myelin basic protein(MBP),and heat shock protein 70(HSP70)before and after treatment were compared between the two groups.Adverse reactions in both groups were recorded.Results The total effective rate was 90.91％in the treatment group,which was significantly higher than 76.36％in the control group(P＜0.05).After treatment,the MMSE score,MoCA score and BI as well as serum levels of ACh,DA,NE,5-HT and HSP70 in the treatment group were significantly higher than those in the control group,while the NIHSS score and serum levels of NSE,VILIP-1 and MBP were significantly lower than those in the control group(P＜0.05).The total incidence rate of adverse reactions in the treatment group and the control group was 12.73％and 9.09％respectively,which showed no significant between-group difference(P＞0.05).Conclusion Four traditional Chinese drugs for reinforcing kidney combined with Tongqiao Huoxue Decoction can promote the secretion of cognition-related neurotransmitters in patients with PSCI,accelerate the repair of neurological damage,and safety is relatively high.

Ferroptosis has been shown to mediate the development of fibrosis. Polyphyllin VII (PP7), a bioactive component of Paris polyphylla, exhibits potent anti-inflammatory activity and can significantly alleviate liver fibrosis. In this study, treatment with PP7 significantly inhibited the proliferation and activation of hepatic stellate cells (HSCs), which could be suppressed by a ferroptosis inhibitor. In addition, it promoted HSC ferroptosis by suppressing glutathione (GSH) peroxidase 4 (GPX4) and enhanced the expression of CX3C chemokine ligand 1 (CX3CL1). Depletion of CX3CL1 attenuated the effects of PP7 on the activation and ferroptosis of HSCs and the expression of GPX4. Notably, CX3CL1 directly interacted with GPX4, triggering HSC ferroptosis. The transcription factor hypermethylated in cancer 1 (Hic1), which binds to the Cx3cl1 promoter, increased the expression of CX3CL1. Its absence resulted in downregulation of CX3CL1, suppressing the GPX4-dependent ferroptosis of PP7-treated HSCs and promoting their activation. HIC1 was found to directly interact with PP7 at the GLY164 site. Co-culture experiments showed that PP7-induced HSC ferroptosis attenuated macrophage recruitment by regulating inflammation-related genes. HSC-specific inhibition of HIC1 counteracted PP7-induced collagen depletion and HSC ferroptosis in vivo. These findings suggest that PP7 induces HSC ferroptosis through the HIC1/CX3CL1/GPX4 axis.

Pristimerin, which is one of the compounds present in Celastraceae and Hippocrateaceae, has antitumor effects. However, its mechanism of action in esophageal squamous cell carcinoma (ESCC) remains unclear. This study aims to investigate the efficacy and mechanism of pristimerin on ESCC in vitro and in vivo. The inhibitory effect of pristimerin on cell growth was assessed using trypan blue exclusion and colony formation assays. Cell apoptosis was evaluated by flow cytometry. Gene and protein expressions were analyzed through quantitative reverse transcription-polymerase chain reaction (qRT-PCR), Western blotting, and immunohistochemistry. RNA sequencing (RNA-Seq) was employed to identify significantly differentially expressed genes (DEGs). Cell transfection and RNA interference assays were utilized to examine the role of key proteins in pristimerin?s effect. Xenograft models were established to evaluate the antitumor efficiency of pristimerin in vivo. Pristimerin inhibited cell growth and induced apoptosis in ESCC cells. Upregulation of Noxa was crucial for pristimerin-induced apoptosis. Pristimerin activated the Forkhead box O3a (FoxO3a) signaling pathway and triggered FoxO3a recruitment to the Noxa promoter, leading to Noxa transcription. Blocking FoxO3a reversed pristimerin-induced Noxa upregulation and cell apoptosis. Pristimerin treatment suppressed xenograft tumors in nude mice, but these effects were largely negated in Noxa-KO tumors. Furthermore, the chemosensitization effects of pristimerin in vitro and in vivo were mediated by Noxa. This study demonstrates that pristimerin exerts an antitumor effect on ESCC by inducing AKT/FoxO3a-mediated Noxa upregulation. These findings suggest that pristimerin may serve as a potent anticancer agent for ESCC treatment.
Forkhead Box Protein O3/genetics* ; Humans ; Apoptosis/drug effects* ; Esophageal Squamous Cell Carcinoma/physiopathology* ; Esophageal Neoplasms/physiopathology* ; Pentacyclic Triterpenes ; Animals ; Cell Line, Tumor ; Proto-Oncogene Proteins c-bcl-2/genetics* ; Mice ; Signal Transduction/drug effects* ; Mice, Nude ; Cell Proliferation/drug effects* ; Triterpenes/pharmacology* ; Xenograft Model Antitumor Assays ; Mice, Inbred BALB C ; Male ; Gene Expression Regulation, Neoplastic/drug effects*

Objective:To investigate the correlation between serum neuron-specific enolase (NSE) levels and poor neurological outcomes in cardiac arrest (CA) patients supported by veno-arterial extracorporeal membrane oxygenation (VA-ECMO).Methods:This retrospective analysis was conducted on adult CA patients treated with VA-ECMO at Hangzhou First People's Hospital Affiliated to Westlake University School of Medicine, and Second Affiliated Hospital Zhejiang University School of Medicine, from December 2018 to February 2024. General clinical data and serial serum NSE levels at 24, 48, and 72 h after ECMO initiation were collected. Based on the Glasgow-Pittsburgh Cerebral Performance Category (CPC) at discharge, patients were divided into poor neurological outcome group (CPC 3-5) and good neurological outcome group (CPC 1-2). Differences in serum NSE levels between the two groups were compared. The accuracy of serum NSE levels at three time points in predicting poor neurological outcomes in CA patients was assessed via receiver operating characteristic curves, and the optimal cut-off values were determined by the Youden index. Multivariate logistic regression analysis was performed to determine the relationship between serum NSE levels and poor neurological outcomes. Subgroup analysis was based on age, sex, location of CA, and extracorporeal cardiopulmonary resuscitation (ECPR).Results:A total of 120 eligible CA patients were included, with 88 patients (73.3%) having poor neurological outcomes at discharge. Serum NSE levels at 24, 48, and 72 h after ECMO initiation were higher in the poor outcome group compared to the good outcome group (all P<0.05). The serum NSE level at 72 h had the highest accuracy in predicting poor outcomes, with an area under the curve (AUC) of 0.91 (95% CI: 0.85-0.96), and a cut-off value of 42.0 μg/L. The AUCs for 24 and 48 h were 0.78 (95% CI: 0.69-0.86) and 0.87 (95% CI: 0.80-0.94), with cut-off values of 70.6 μg/L and 64.5 μg/L, respectively. Multivariate logistic regression analysis suggested that the serum NSE level at 72 h was associated with poor outcomes ( P<0.05), and an NSE level >42.0 μg/L was an independent risk factor for poor outcomes ( OR=20.29, 95% CI: 2.90-92.15). Subgroup analysis showed that serum NSE level at 72 h was an independent risk factor for poor neurological outcomes in CA patients aged<60 years old, male or female, out-of-hospital or in-hospital CA, and whether to perform ECPR (all P<0.05). Conclusion:Elevated serum NSE levels at 72 h after VA-ECMO initiation are associated with poor neurological outcomes in CA patients, with the cut-off value of 42.0 μg/L.