Ferroptosis, a programmed cell death modality discovered and defined in the last decade, is primarily induced by iron-dependent lipid peroxidation. At present, it has been found that ferroptosis is involved in various physiological functions such as immune regulation, growth and development, aging, and tumor suppression. Especially its role in tumor biology has attracted extensive attention and research. Breast cancer is one of the most common female tumors, characterized by high heterogeneity and complex genetic background. Triple negative breast cancer (TNBC) is a special type of breast cancer, which lacks conventional breast cancer treatment targets and is prone to drug resistance to existing chemotherapy drugs and has a low cure rate after progression and metastasis. There is an urgent need to find new targets or develop new drugs. With the increase of studies on promoting ferroptosis in breast cancer, it has gradually attracted attention as a treatment strategy for breast cancer. Some studies have found that certain compounds and natural products can act on TNBC, promote their ferroptosis, inhibit cancer cells proliferation, enhance sensitivity to radiotherapy, and improve resistance to chemotherapy drugs. To promote the study of ferroptosis in TNBC, this article summarized and reviewed the compounds and natural products that induce ferroptosis in TNBC and their mechanisms of action. We started with the exploration of the pathways of ferroptosis, with particular attention to the System X_c^--cystine-GPX4 pathway and iron metabolism. Then, a series of compounds, including sulfasalazine (SAS), metformin, and statins, were described in terms of how they interact with cells to deplete glutathione (GSH), thereby inhibiting the activity of glutathione peroxidase 4 (GPX4) and preventing the production of lipid peroxidases. The disruption of the cellular defense against oxidative stress ultimately results in the death of TNBC cells. We have also our focus to the realm of natural products, exploring the therapeutic potential of traditional Chinese medicine extracts for TNBC. These herbal extracts exhibit multi-target effects and good safety, and have shown promising capabilities in inducing ferroptosis in TNBC cells. We believe that further exploration and characterization of these natural compounds could lead to the development of a new generation of cancer therapeutics. In addition to traditional chemotherapy, we discussed the role of drug delivery systems in enhancing the efficacy and reducing the toxicity of ferroptosis inducers. Nanoparticles such as exosomes and metal-organic frameworks (MOFs) can improve the solubility and bioavailability of these compounds, thereby expanding their therapeutic potential while minimizing systemic side effects. Although preclinical data on ferroptosis inducers are relatively robust, their translation into clinical practice remains in its early stages. We also emphasize the urgent need for more in-depth and comprehensive research to understand the complex mechanisms of ferroptosis in TNBC. This is crucial for the rational design and development of clinical trials, as well as for leveraging ferroptosis to improve patient outcomes. Hoping the above summarize and review could provide references for the research and development of lead compounds for the treatment for TNBC.

Traditional Chinese medicine (TCM) is a well-accepted therapy for atopic dermatitis (AD). However, there are currently no evidence-based guidelines integrating TCM and Western medicine for the treatment of AD, limiting the clinical application of such combined approaches. Therefore, the China Association of Chinese Medicine initiated the development of the current guideline, focusing on key issues related to the use of TCM in the treatment of AD. This guideline was developed in accordance with the principles of the guideline formulation manual published by the World Health Organization. A comprehensive review of the literature on the combined use of TCM and Western medicine to treat AD was conducted. The findings were extensively discussed by experts in dermatology and pharmacy with expertise in both TCM and Western medicine. This guideline comprises 23 recommendations across seven major areas, including TCM syndrome differentiation and classification of AD, principles and application scenarios of TCM combined with Western medicine for treating AD, outcome indicators for evaluating clinical efficacy of AD treatment, integration of TCM pattern classification and Western medicine across disease stages, daily management of AD, the use of internal TCM therapies and proprietary Chinese medicines, and TCM external treatments. Please cite this article as: Du XR, Wu MY, Tao MC, Lin Y, Gu CY, Wu MF, Cao Y, Chen DC, Li W, Wang HW, Wang Y, Wang Y, Lu HZ, Liu X, Su XF, Li FL. Clinical practice guidelines for the diagnosis and treatment of atopic dermatitis with integrative traditional Chinese and Western medicine. J Integr Med. 2025; 23(6):641-653.
Dermatitis, Atopic/drug therapy* ; Humans ; Medicine, Chinese Traditional/methods* ; Integrative Medicine ; Drugs, Chinese Herbal/therapeutic use* ; Practice Guidelines as Topic

OBJECTIVE: Observational studies have shown inconsistent associations of loneliness or social isolation (SI) with ischemic heart disease (IHD), with unknown mediators. METHODS: Using data from genome-wide association studies of predominantly European ancestry, we performed a bidirectional two-sample Mendelian Randomization (MR) study to estimate causal effects of loneliness ( N = 487,647) and SI traits on IHD ( N = 184,305). SI traits included whether individuals lived alone, participated in various types of social activities, and how often they had contact with friends or family ( N = 459,830 to 461,369). A network MR study was conducted to evaluate the mediating roles of 20 candidate mediators, including metabolic, behavioral and psychological factors. RESULTS: Loneliness increased IHD risk ( OR= 2.129; 95% confidence interval [ CI]: 1.380 to 3.285), mediated by body fat percentage, waist-hip ratio, total cholesterol, and low-density lipoprotein cholesterol. For SI traits, only fewer social activities increased IHD risk ( OR= 1.815; 95% CI: 1.189 to 2.772), mediated by hypertension, high-density lipoprotein cholesterol, triglycerides, fasting insulin, and smoking cessation. No reverse causality of IHD with loneliness and SI was found. CONCLUSION These findings suggested more attention should be paid to individuals who feel lonely and have fewer social activities to prevent IHD, with several mediators as prioritized targets for intervention.
Loneliness/psychology* ; Humans ; Mendelian Randomization Analysis ; Social Isolation ; Myocardial Ischemia/etiology* ; Male ; Female ; Middle Aged ; Genome-Wide Association Study ; Risk Factors ; Aged

Nutritional therapy is a core component of critically ill patient management,and the enteral route has become the preferred method due to its dual roles of nutrition and non-nutrition. The use of vasoactive medications makes enteral nutrition decisions more challenging for these patients. This review systematically examines the pathophysiological effects of vasoactive medications on gastrointestinal tract of critically ill patients,the current value and safety of enteral nutrition in this patient's population,summarizes the optimal strategies for implementing enteral nutrition in these patients for clinical reference.

Modern Chinese medicine studies have confirmed that the interaction between traditional Chinese medicine(TCM)and intestinal flora is the key to the treatment of diseases with tradi-tional Chinese medicine.This interplay includes such activities as:traditional Chinese medicine can be metabolized by intestinal flora into effective components with different biological activities from its precursors;TCM chemicals improve the composition of gut microbiota,consequently ameliorating its dysfunction as well as associated pathological conditions;and gut microbiota mediate the interactions between the multiple chemicals in TCM.There-fore,it becomes an important way to understand the modern sci-entific connotation of traditional Chinese medicine theory to study the pharmacological mechanism of the efficacy of traditional Chi-nese medicine by targeting Gut microbiota.

This study aimed to investigate the potential role of Colquhounia Root Tablets against bone destruction in rheumatoid arthritis(RA) and its molecular mechanism. The study used ultra-performance liquid chromatography-mass spectrometry to analyze the major components of Colquhounia Root Tablets and predicted its candidate target gene set based on the major components. The key targets of RA bone destruction were obtained through GeneCards and the Database of Genetics and Medical Literature(OMIM), protein-protein interaction(PPI) network was constructed, and the key targets were identified by topological analysis. The molecular mechanism of Colquhounia Root Tablets against RA bone destruction was further revealed using Gene Ontology(GO) and Kyoto Encyclopedia of Genes and Genomes(KEGG) enrichment analysis. The effects of Colquhounia Root Tablets on macrophage viability was assessed by MTS assay and screened for non-toxic concentrations. A model of receptor activator of nuclear factor-κB(RANKL) induced osteoclast differentiation in vitro was constructed. Colquhounia Root Tablets were used to observe the formation and differentiation of osteoclasts by tartrate-resistant acid phosphatase(TRAP) staining and fibrous actin(F-actin) staining, and the effects of Colquhounia Root Tablets on the changes of core target proteins in the osteoclast differentiation system were detected by immunofluorescence and Western blot. The results showed that the main components of Colquhounia Root Tablets included 14 compounds such as triptolide, celastrol, and triptophenolide. Further network analysis revealed that heat-shock protein 90(HSP90) was the key target gene of Colquhounia Root Tablets for anti-RA bone destruction. TRAP staining and F-actin staining showed that the number and area of TRAP-positive polymorphonuclear cells, as well as actin rings, were reduced in a dose-dependent manner after the intervention of Colquhounia Root Tablets(P<0.01). Western blot results showed that the expression of HSP90 protein was significantly reduced after intervention with Colquhounia Root Tablets at 20 and 40 μg·mL~(-1)(P<0.01); Colquhounia Root Tablets at 10 μg·mL~(-1) could significantly decrease the expression of necrosis factor receptor associated molecule 6(TRAF6) and nuclear factor of activated T cells 1(NFATc1) proteins(P<0.01); moreover, all doses of Colquhounia Root Tablets significantly reduced the expression of osteoclast differentiation marker proteins matrix metalloproteinase 9(MMP9) and cathepsin K(CTSK)(P<0.01).Immunofluorescence results further confirmed that Colquhounia Root Tablets significantly inhibited HSP90 and CTSK levels, as well as NFATc1 activation in osteoblasts. In conclusion, the present study confirmed that Colquhounia Root Tablets may inhibit RANKL-induced osteoclast differentiation by regulating the key target of HSP90, thus exerting an anti-RA bone destruction effect, which will provide a new idea for Colquhounia Root Tablets to prevent and treat bone destruction in rheumatoid arthritis.
Osteoclasts/metabolism* ; Mice ; Animals ; Cell Differentiation/drug effects* ; HSP90 Heat-Shock Proteins/genetics* ; Drugs, Chinese Herbal/chemistry* ; Plant Roots/chemistry* ; Humans ; Arthritis, Rheumatoid/physiopathology* ; Protein Interaction Maps/drug effects*

Aim To study the effect of salidroside on the proliferation, migration, invasion and apoptosis of human highly metastatic liver cancer cells ( 97 H cells) . Methods Multifunctional cell analyzer was used to determine the effect of salidroside on the proliferation of 97H cells. Scratch assay was used to determine the effect of salidroside on the migration ability of 97H cells. Transwell assay was used to determine the effect of salidroside on the invasion ability of 97 H cells. Inverted microscope was used to observe the effect of salidroside on the morphology of 97H cells. Transmission electron microscope was employed to observe the effect of salidroside on mitochondria in 97 H cells. Flow cytometry was used to analyze the effect of salidroside on apoptosis and cycle distribution of 97 H cells. q-PCR was used to determine the effect of salidroside on related apoptosis genes in 97H cells.Western blot was used to determine the effect of salidroside on related migration, invasion and apoptosis proteins in 97H cells. Results Compared to blank group, salidroside treatment inhibited the proliferation, migration and invasion of 97H cells, and induced apoptosis of 97H cells. Salidroside could up-regulate the relative expression of Caspase-3 (P <0.05). Salidroside could up-regulate the levels of E-cad, Bax, Caspase-3 and Caspase-9 proteins (P <0.05), and down-regulate the levels of N-cad, Girdin and Bcl-2 proteins (P < 0. 05 ). Conclusions Salidroside has inhibitory effects on the proliferation, migration and invasion of 97H cells, and induces apoptosis of 97H cells through mitochondrial pathway.

Cold agglutinins(CA),autoantibodies against the antigen I or i on the surface of red blood cells,are mainly of IgM class,and the majority have κ light chains.They can lead to red blood cell agglutination at decreased body temperature and are usually associated with infections,drug reactions,autoimmune diseases,and hematological malignancies.However,solid tumors with CA are rare.We reported two cases of CA in the peripheral blood of patients with solid tumors.Peripheral complete blood cell count of the patients at admission showed reduced erythrocyte count and hematocrit,mismatching between erythrocyte count and hemoglobin,abnormally elevated levels of mean corpuscular hemoglobin and mean cell hemoglobin concentration.Peripheral blood smear showed erythrocyte aggregation.After the sample was preheated at 37 ℃ for 30 min,the reversibility of red blood cell aggregation was observed,and the erythrocyte parameters were corrected.
Humans ; Autoantibodies/isolation & purification* ; Female ; Breast Neoplasms/immunology* ; Ovarian Neoplasms/immunology*

This article uses the "behavioural and social drivers of vaccination" model released by the World Health Organization (WHO) in 2022 to analyze influenza vaccine policy documents issued by the state and governments. This indicates that the current influenza vaccination policy in China has paid some attention to "publicity and mobilization", but it still pays insufficient attention to "vaccination convenience". It is recommended to continue to strengthen publicity and mobilization, explore ways to improve the convenience of vaccination, formulate corresponding plans to improve the convenience of vaccination, scientifically set vaccination rate targets, and encourage areas with conditions to carry out free vaccination projects for key populations.

The latest guideline about ulcerative colitis (UC) clinical practice stresses that mucosal healing, rather than anti-inflammation, is the main target in UC clinical management. Current mucosal dysfunction mainly closely relates to the endoscopic intestinal wall (mechanical barrier) injury with the imbalance between intestinal epithelial cells (IECs) regeneration and death, as well as tight junction (TJ) dysfunction. It is suggested that biological barrier (gut microbiota), chemical barrier (mucus protein layer, MUC) and immune barrier (immune cells) all take part in the imbalance, leading to mechanical barrier injury. Lots of experimental studies reported that acupuncture and moxibustion on UC recovery by adjusting the gut microbiota, MUC and immune cells on multiple targets and pathways, which contributes to the balance of IEC regeneration and death, as well as TJ structure recovery in animals. Moreover, the validity and superiority of acupuncture and moxibustion were also demonstrated in clinic. This study aims to review the achievements of acupuncture and moxibustion on mucosal healing and analyse the underlying mechanisms.
Rats ; Animals ; Colitis, Ulcerative/metabolism* ; Moxibustion ; Rats, Sprague-Dawley ; Acupuncture Therapy ; Acupuncture