Objective To introduce the causes of accidents and the diagnosis and treatment of two patients with radiation-induced skin injury admitted to our hospital in 2023, and to provide a reference for the clinical treatment of subsequent radiation-induced skin injury. Methods The clinical treatment process of two patients with acute skin injury caused by external radiation exposure were summarized and analyzed. Results The exposure history of the two patients was reconstructed, the flaw detection scenario was simulated, the biological dose and hand skin exposure dose were estimated, and the infrared thermal imaging device was used for dynamic monitoring. A comprehensive analysis was conducted based on clinical manifestations and other data. The diagnosis of “Xie” was excessive exposure combined with acute radiation-induced skin injury on both hands (Grade IV for the right hand palm, index finger, and middle finger and Grade II for the left hand little finger). The diagnosis of “Hao” was acute radiation-induced skin injury on both hands (Grade I). The two patients received different clinical treatment measures: “Xie” was treated with both local and systemic therapies, while “Hao” was mainly treated with systemic therapy. Conclusion After systematic and effective treatment, the radiation-induced skin injuries healed in both patients.

Objective: To compare the Reveos automated blood processing system with the current method, and to evaluate the feasibility and validity of using the Reveos system for blood component preparation. Methods: Forty units of 400 mL whole blood samples were divided into two groups: 2C group (for two-component preparation) and 3C group (for three-component preparation). Each group was further divided into a Reveos subgroup and a control subgroup. Blood components were prepared using the Reveos system and the current centrifugation method respectively. The 2C group yielded suspended red blood cells and plasma, while the 3C group yielded suspended red blood cells, plasma, and platelets. Key quality indicators for red blood cells, plasma, and platelets were measured before and after separation. Inter-group differences were analyzed using SPSS 25.0. Results: The trend of changes in the main performance indicators of red blood cells, plasma, and platelets before and after separation was generally consistent between the Reveos group and the control group, with no significant differences for most performance indicators. The Reveos system outperformed the current method in several aspects: in the 3C group, the hematocrit (Hct) was significantly higher in the Reveos group than in the control group [(62.82%±1.64%) vs (53.62%±3.04)%, P<0.001]; the white blood cell count in red blood cell suspensions was significantly lower than that in the control group [(3.37±1.42)×10 /L vs (8.42±2.30)×10 /L, P<0.001]; plasma yield was 27.5% higher than that in the control group [(183.90±17.37) mL vs (144.28±20.53) mL, P<0.001]; and the platelet activation rate was significantly lower than that in the control group [(21.97±14.25)% vs (34.73±11.92)%, P=0.044]. Conclusion: The Reveos system demonstrates good consistency with the current method in preparing blood components, and outperforms the current method in terms of leukocyte reduction and red blood cell concentration.

Objective: To develop a RHCE genotyping assay based on kompetitive allele-specific PCR (KASP) and assess its clinical accuracy for RhCE blood group determination. Methods: KASP primers were designed to interrogate three RHCE loci: the 109 bp insertion/deletion in intron 2, c. 307T>C, and c. 676C>G. A total of 1 194 RhD-positive inpatients from Chengdu were typed by both KASP genotyping and manual tube serology. Discordant samples (n=10) were retested by both methods and further resolved by Sanger sequencing. An additional 377 cases were tested for the c. 48C>G locus to evaluate the predictive accuracy of individual loci and combined locus testing for RhC antigen. Results: Genotyping concordance with serology was 100.0% for both the c. 676C>G locus (RhE/Rhe) and the c. 307T>C locus (Rhc). For RhC prediction using the 109 bp insertion, overall accuracy was 99.7% (1 191/1 194); the 3 discordant cases were confirmed by Sanger sequencing to be false negatives attributable to 109 bp deletion in intron 2. Testing the c. 48C>G allele for RhC prediction yielded 7 false positives, with an accuracy of 98.1% (370/377). RhC antigen status was determined by combining the 109 bp insertion and the c. 48C allele. After excluding 10 samples with inconsistent results between the two loci, the accuracy reached 100% in the remaining 367 samples. When both loci were applied in combination, accuracy reached 100% in the 367 cases with concordant results. Among the 1 194 patients, CCee (45.8%) and CcEe (31.7%) were the most common RhCE phenotypes. The e antigen had the highest positivity rate (92.2%), and the Ce haplotype was the most frequent (66.9%). Conclusion: The KASP-based RHCE genotyping method achieves high accuracy for clinical RhCE typing. Combining the 109 bp insertion/deletion with the c. 48C allele significantly improves RhC antigen prediction compared with either locus alone. This method was applied to RhCE genotyping of 1 194 RhD-positive inpatients in Chengdu, providing local RhCE phenotype and haplotype distribution data to support RhCE-matched transfusion practice.

Background/Aims: Liver transplantation (LT) following total hepatectomy is a life-saving treatment for hepatocellular carcinoma (HCC). The HCC recurrence after LT hinders the effectiveness of the procedure. The objective of this study is to develop a pre-operative risk stratification model based on a liquid biopsy. Methods: We conducted a comprehensive multi-omics study of 260 HCC patients from three centers, including clinical data, low-coverage whole-genome sequencing of cell-free DNA (cfDNA) from plasma, as well as whole-exome, single-nucleus RNA, and spatial transcriptomics from matched tumor and non-tumor tissues. Results: We identified cfDNA-derived copy number alteration (CNA) signatures associated with post-transplant recurrence. By integrating cfDNA-derived CNA profiles with single-cell transcriptomic data, we traced recurrence-associated cfDNA to a distinct subpopulation of malignant cells within the primary tumor. These cells were embedded in a pro-metastatic microenvironment of specialized endothelial subtypes and cancer-associated fibroblasts. Notably, most recurrence-associated lesions were detectable in cfDNA prior to liver transplantation (LT). Building on these insights, we developed the ZJU Criteria based on CNA fragments and tumor markers, a pre-LT risk prediction tool that integrates conventional clinical factors with cfDNA-derived CNA signatures, and validated it using internal and independent external cohorts. Conclusion Our findings suggest that post-transplant recurrence commonly originates from advanced subclones that emerge late during tumor evolution. The ZJU Criteria provides an accurate, non-invasive strategy that significantly improves pre-LT risk stratification and clinical decision-making for patients with HCC.

Lung transplantation is currently the only effective treatment for end-stage lung disease. However, the field of lung transplantation still faces numerous challenges, including donor shortage, primary graft dysfunction, rejection, infection and others. In 2025, scholars worldwide have made remarkable progress in clinical research on lung transplantation. This article systematically reviews the cutting-edge developments in clinical research on lung transplantation in 2025, focusing on the application of novel evaluation tools in donor lung screening, optimization of lung perfusion techniques, exploration of extracorporeal membrane oxygenation and robot-assisted minimally invasive surgery, as well as mechanistic research and intervention strategies for primary graft dysfunction, acute kidney injury and chronic lung allograft dysfunction. Meanwhile, hot topics such as the management of special populations, prevention and control of postoperative infections, and improvement of quality of life are summarized. This review aims to conclude the important annual research findings and provide references for the clinical practice and research development of lung transplantation in China.

Nicotinic acetylcholine receptors (nAChRs) are pentameric ligand-gated ion channels (pLGICs) that mediate rapid cholinergic synaptic transmission throughout the central and peripheral nervous systems. These receptors are integral to neuromuscular junction signaling, autonomic regulation, cognitive learning, reward-related behavior, and neuroplasticity. The nAChR family exhibits remarkable functional diversity through combinatorial assembly of seventeen identified subunits (α1-α10, β1-β4, γ, δ, and ε). Among these, the α9 subunit occupies a distinctive phylogenetic position, exhibiting greater sequence divergence from other neuronal α subunits and possessing unique biochemical properties that distinguish it from all other family members. α9 can form homopentamers and also co-assemble with the α10 subunit to form functional heteropentamers, primarily in (α9)₂(α10)₃ and (α9)₃(α10)₂ stoichiometries. This dual assembly strategy generates functional heterogeneity, as distinct subunit compositions confer differential ion permeation, ligand sensitivity, and desensitization kinetics. The structural determinants governing this stoichiometric variability remain incompletely resolved, representing a critical gap in our mechanistic understanding. Unlike most other nAChR subtypes, traditional agonists of nAChRs (such as nicotine) elicit virtually no agonistic effect on α9* nAChRs (α9-containing receptors, including α9 homopentamers and α9α10 heteropentamers). This pharmacological divergence reflects structural differences within the orthosteric site, particularly in regions at complementary subunit interfaces. As cation-selective channels, α9* nAChRs exhibit high permeability to Ca²⁺. In cochlear outer hair cells, α9α10 nAChRs mediate cholinergic efferent modulation by the medial olivocochlear (MOC) bundle. Acetylcholine-evoked Ca²⁺ influx activates functionally coupled SK2 potassium channels, generating net hyperpolarization that dampens electromechanical amplification through a tightly constrained signaling microdomain. This Ca²⁺-dependent excitatory-to-inhibitory conversion exemplifies sophisticated sensory gain control, and its disruption contributes to noise-induced hearing loss, age-related hearing loss, and tinnitus. Beyond canonical ionotropic signaling, α9* nAChR engages metabotropic transduction pathways. In macrophages, receptor activation modulates cytokine production and inflammatory responses. In keratinocytes, it regulates wound healing by modulating cell migration and differentiation. In dorsal root ganglion sensory neurons, α9* signaling contributes to nociceptive processing and inflammatory hyperalgesia. This functional pleiotropy, spanning both ionotropic signaling and metabotropic transduction, positions α9* nAChR as an exemplary model for investigating signal polymorphism within the pLGIC superfamily. Pathophysiologically, α9* nAChR dysfunction is implicated across multiple organ systems. In the auditory system, disruption of α9α10 nAChR-mediated MOC efferent feedback impairs cochlear gain control, predisposing to noise-induced synaptopathy and age-related hearing loss. In immune cells, dysfunctional α9* nAChR signaling disrupts cholinergic anti-inflammatory pathway activity, exacerbating pro-inflammatory responses. In the peripheral sensory system, aberrant α9* nAChR signaling has been implicated in neuropathic and inflammatory pain states. In skin, impaired receptor function compromises keratinocyte migration and re-epithelialization through disrupted signaling pathways, leading to chronic wound healing defects and inflammation. These pathophysiological associations have catalyzed pharmacological interest, yielding promising chemical entities including α‑conotoxins, small-molecule antagonists/agonists, and allosteric modulators.α-Conotoxin peptides, in particular, demonstrate remarkable subunit selectivity and potent antinociceptive effects in preclinical pain models. However, therapeutic translation faces substantial challenges: the broad tissue distribution of α9* nAChR risks on-target adverse effects in non-target organs; pronounced species differences between rodent and human receptors complicate preclinical validation; and the complexity of ionotropic-metabotropic signaling crosstalk demands pharmacological strategies that extend beyond conventional orthosteric agonism or antagonism. Looking forward, integrating cryo-electron microscopy of full-length receptors in distinct conformational states with single-channel electrophysiology and systems-level circuit analysis promises to illuminate the molecular mechanisms governing α9* nAChR function and regulation. The development of signal pathway-biased ligands and tissue-selective delivery strategies may ultimately harness the therapeutic potential of this receptor while mitigating safety liabilities. As a paradigm for understanding pLGIC signaling diversification, α9* nAChR research will continue to inform broader questions regarding ion channel evolution, allosteric regulation, and pathophysiological mechanisms of chronic pain and autoimmune inflammatory diseases.

Objective: To investigate the effects of curcumin on the biological behavior of oral squamous cell carcinoma (OSCC) cells and its potential molecular mechanisms, as well as to provide experimental evidence for the application of curcumin in the prevention and treatment of OSCC. Methods: All animal experiments in this study were approved by the Institutional Animal Welfare and Ethics Committee and strictly adhered to relevant animal ethics guidelines. Potential intersecting targets of curcumin and OSCC were screened using TCMSP, SwissTargetPrediction, DrugBank, and GeneCards databases, followed by construction of a protein-protein interaction network and gene ontology(GO) /Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analyses. Scratch and clone formation experiments were conducted using CAL-27 and SCC-9 cells to detect the effect of curcumin on cell migration and proliferation ability. Combining RNA sequencing analysis of differentially expressed genes, and verifying the changes in mRNA and protein expression of key cellular molecules by curcumin through real-time fluorescence quantitative PCR and Western blot, respectively. Simultaneously establish a CAL-27 xenograft BALB/c nude mouse transplant tumor model and use immunohistochemistry to detect the effect of curcumin treatment on the expression of related proteins in the transplant tumor tissue. Results: A total of 178 intersecting targets were identified, mainly enriched in the PI3K/AKT signaling pathway and lipid metabolism-related pathways. Curcumin significantly inhibited migration and colony formation of CAL-27 and SCC-9 cells in vitro. Transcriptomic analysis identified 828 differentially expressed genes enriched in lipid metabolism and PI3K/AKT pathways. Real-time fluorescence quantitative PCR showed downregulation of PIK3CA, CCND1, BCL2, and FASN, while western blot demonstrated decreased expression of p-AKT and FASN. In vivo, curcumin markedly suppressed tumor growth and reduced the expression of Ki-67, BCL2, and p-AKT in tumor tissues. Conclusion Curcumin may inhibit the migration and proliferation of OSCC cells by regulating the PI3K/AKT signaling pathway and the expression of lipid metabolism-related genes.

Lung cancer constitutes the most prevalent and lethal malignant tumor in China. Approximately 85% of lung cancer diagnoses correspond to the non-small cell histological subtype [non-small cell lung cancer (NSCLC)]. Despite surgery being the mainstay for early-stage disease, postoperative recurrence remains high and adjuvant chemotherapy offers limited benefit. In recent years, targeted therapy has demonstrated substantial advantages in driver mutation-positive NSCLC. To this end, the Lung Cancer Medical Education Committee of the Chinese Medical Education Association developed guidelines based on a systematic review of evidence through November 2025, using the Grading of Recommendations, Assessment, Development and Evaluations (GRADE) approach and a modified Delphi method. Focusing on epidermal growth factor receptor (EGFR) and anaplastic lymphoma kinase (ALK), and addressing ROS proto-oncogene 1 (ROS1), B-Raf proto-oncogene serine/threonine kinase (BRAF) V600E mutation, and mesenchymal-epithelial transition factor (MET) exon 14 (METex14) skipping, the guideline covers molecular testing, neoadjuvant/adjuvant therapy, perioperative strategies, minimal residual disease monitoring, and postoperative surveillance. It defines testing requirements, specifies stage-directed and subtype-specific treatments, and standardizes minimal residual disease monitoring. These recommendations emphasize precision and feasibility to improve survival and quality of life.

Breast cancer is one of the most common cancers in the world， and its incidence rate is also rising in China and tends to happen in younger age groups. The classical Wnt/β-catenin signaling pathway is an important target in the treatment of breast cancer， playing a key role in the whole process of breast cancer development by regulating the expression of related signal proteins and genes. Traditional Chinese medicine has a profound history and practical experience in the treatment of malignant tumors， and the development of modern technology further highlights the therapeutic advantages of traditional Chinese medicine， which has multiple targets and components. Research shows that Chinese medicine can effectively slow down the proliferation of breast cancer cells by regulating the Wnt/β-catenin signaling pathway， and has a significant inhibitory effect on the development of breast cancer. Based on this， this paper summarized domestic and foreign relevant studies on the regulation of the Wnt/β-catenin signaling pathway with traditional Chinese medicine in the treatment of breast cancer， analyzed the mechanism of traditional Chinese medicine treating breast cancer by intervening in this signaling pathway， and summarized 44 different types of traditional Chinese medicine monomers， including terpenes （triptolide， andrographolide， etc.）， flavonoids （scutellarin， sinensetin， etc.）， polysaccharides （Angelica sinensis polysaccharides， etc.）， phenols （curcumin， polydatin， etc.）， and alkaloids （lycorine， etc.）. In addition， there are 3 traditional Chinese medicines （Ganoderma lucidum， Radix actinidia chinensis， and Antrodia camphorata）， 1 group of medicine pairs （Trionycis Carapax-Zedoary Turmeric）， and 8 traditional Chinese medicine formulas （Compound Tubeimu， Huangqi Jiedu Tang， Xihuang Wan， Liuwei Dihuang Wan， Jiazhu Tang， Aiduqing Fang， Sini San， and compound Kushen injection）. By regulating the Wnt/β-catenin signaling pathway and its key molecules， these single herbs， monomers， and compound herbs can reverse the epithelial mesenchymal transformation process， reduce the activity of stem cells， and inhibit the growth and metastasis of cancer cells. Besides， it can also enhance the sensitivity of drugs and radiotherapy and combat breast cancer， providing a new perspective for drug development and treatment strategies for breast cancer.

Prostate cancer is a malignant tumor that primarily arises from the epithelial tissue of the prostate in men. With the aggravation of population aging in China， the incidence rate of this disease has been continuously rising. Although the exact cause of prostate cancer remains unclear， it has been proven to be closely related to various factors， including individual genetic susceptibility， genetic mutations， dietary habits， and lifestyle. Research has shown that abnormal activation of the Wnt/β-catenin signaling pathway also plays an important role in the occurrence and development of prostate cancer. Multiple experimental results have revealed that traditional Chinese medicine （TCM）， with its multi-target and multi-stage mechanisms of action， exerts significant regulatory effects on key biological processes such as proliferation， migration， invasion， angiogenesis， and epithelial-mesenchymal transition （EMT） of prostate cancer cells. TCM has shown excellent potential in preventing prostate cancer progression and improving patient prognosis and has become a research focus in prostate cancer treatment in recent years. Based on this， this study reviewed the research on the regulation of the Wnt/β-catenin signaling pathway by TCM in the treatment of prostate cancer at home and abroad. It analyzed the mechanisms by which TCM intervention exerts anti-prostate cancer effects via this signaling pathway， identifying 29 different types of active ingredients in TCM， including alkaloids （e.g.， capsaicin， berberine）， flavonoids （e.g.， icariin and hyperoside）， polyphenols （e.g.， gastrodin and honokiol）， terpenes （e.g.， oridonin）， quinones （e.g.， aloe-emodin）， coumarins （e.g.， agrimonolide）， and saponins （e.g.， saikosaponin-d）. Additionally， one TCM medicinal substance （arsenic）， one drug pair （Danggui - Qieyi combination）， and two TCM formulae （Yishen Tonglong Tang and Guben Qingyuan Formula） were included. The study aims to deepen the understanding of the pathological mechanism of prostate cancer and to explore possible therapeutic targets， thereby providing new perspectives and approaches for clinical research and new drug development， and ultimately promoting the advancement and innovation of prostate cancer treatment strategies.