Adeno-associated virus (AAV) vectors have favorable safety and durable transgene expression but are limited in oncology by insufficient tumor specificity and off-target expression. Tumor hypoxia and non-small cell lung cancer (NSCLC)-associated surface ligands offer complementary layers of biological selectivity for more precise gene delivery. This study proposes an NSCLC-directed, hypoxia-responsive AAV architecture that integrates MGS4-guided capsid targeting with dual hypoxia-responsive element (HRE)-gated promoters driving glutamine-modified C-X-C motif chemokine ligand 9-fragment crystallizable region fusion protein (Q-CXCL9-Fc) expression and baculoviral IAP repeat containing 5 (BIRC5)-linked mesothelin (MSLN) silencing. We conceptually designed an AAV vector that combines three layers of NSCLC selectivity: MGS4-guided capsid targeting, hypoxia-gated transcription, and tumor-active promoter control. The capsid displays the MGS4 peptide, isolated by phage display biopanning as a high-affinity ligand for the lung squamous cell carcinoma cell line HCC15 and later shown to internalize into a substantial fraction of NSCLC cell lines and bind a subset of human NSCLC biopsy samples, indicating activity across multiple NSCLC subtypes. The genome encodes Q-CXCL9-Fc under a 4× HRE-cytomegalovirus promoter to sustain C-X-C motif chemokine receptor 3-dependent T-cell recruitment and a miR-30-based short hairpin RNA targeting MSLN under a 4× HRE-BIRC5 promoter to inhibit tumor progression. This architecture is hypothesized to enrich AAV entry into NSCLC lesions via MGS4 while restricting Q-CXCL9-Fc secretion and MSLN silencing to hypoxic, BIRC5-active tumor regions, enabling synergistic enhancement of antitumor immunity and suppression of tumor-intrinsic pathways. The proposed multimodal, hypoxia-responsive AAV platform represents a conceptual precision oncology strategy that couples environmental sensing, tumor-specific transcription, and peptide-defined tropism within a single vector and could inform next-generation NSCLC-directed AAV systems.

Unlike the traditional staging treatment of tumors, the core of “Green Tumor Treatment” is to divide the treatment of tumors into three stages: Hegemony (directly targeting the cancer focus), Kingship (supporting the body’s vital energy and eliminating pathogenic factors), and Imperialism (improving the internal environment), based on the urgency of the tumor and the patient’s physical condition. This approach guides the clinical treatment of tumors. Its treatment system incorporates all minimally invasive and low-damage treatment methods, combining internal and external treatments, traditional Chinese medicine and Western medicine, as well as local and systemic treatments. It aims to maximize treatment outcomes while ensuring the patient’s quality of life, which is highly consistent with the treatment goals for primary liver cancer. This review aims to explore the integrated Traditional Chinese and Western medicine treatment model for primary liver cancer under the guidance of the Green Tumor Treatment concept.

Microbial resistance and oxidative stress are two significant health issues associated with chronic illnesses and therapy failures. The antioxidant and antibacterial properties of Euphorbia cuneata Vahl. aerial component extracts made with various polarity solvents were assessed in this work.

Disc diffusion and minimum inhibitory concentration (MIC) tests were used to evaluate the 1,1-diphenyl-2-picrylhydrazyl radical scavenging activity, total phenolic and flavonoid contents, and antimicrobial activity of n-hexane, toluene, ethanolic, and aqueous extracts against specific ESKAPE pathogens (Staphylococcus aureus, Escherichia coli, Pseudomonas aeruginosa, and Candida albicans). High-performance liquid chromatography and gas chromatography-mass spectrometry were used to further characterize the most active extract.

Compared to the aqueous (IC₅₀ = 51.61 µg/mL), toluene (IC₅₀ = 30.57 µg/mL), and n-hexane (IC₅₀ = 128.15 µg/mL) extracts, the ethanolic extract demonstrated the greatest 1,1-diphenyl-2-picrylhydrazyl radical scavenging activity (97.90 ± 0.8%; IC₅₀ = 28.52 µg/mL). Additionally, it has the highest levels of flavonoids (40.5 ± 1.5 mg luteolin equivalents/g) and phenolic (80.0 ± 0.2 mg gallic acid equivalents/g). While gas chromatography-mass spectrometry found methyl 12-hydroxy-9-octadecenoate (44.39%) as the main volatile molecule, high-performance liquid chromatography analysis identified caffeic acid, pyrogallol, rutin, and 7-hydroxyflavone as important ingredients. The ethanolic extract showed antifungal activity against C. albicans (MIC = 6.25 mg/mL) and moderate antibacterial activity with the lowest MIC values against S. aureus (450 µg/mL) and E. coli (500 µg/mL).

The ethanolic extract of Euphorbia cuneata demonstrated potent in vitro antioxidant activity and moderate antimicrobial effects, primarily attributable to its high phenolic and flavonoid content. These results support its potential as a natural source of bioactive compounds for further development.

Nonalcoholic fatty liver disease (NAFLD) is a prevalent metabolic disorder with a complex pathogenesis. Although epitranscriptomic modifications such as N6-methyladenosine (m6A) have been implicated in NAFLD, the role of N1-methyladenosine (m1A) and its regulators is largely unexplored. Recently, YTHDF1, a well-characterized m6A reader, was also shown to recognize m1A; however, the functional consequences of this dual specificity are unknown. This study aimed to investigate the role of YTHDF1 in NAFLD pathogenesis and to explore whether its function is mediated through recognition of RNA methylation modification on specific target mRNAs.

Expression of YTHDF1 in NAFLD was analyzed in the GEO database. Loss-of-function studies for YTHDF1 were conducted in vivo (high-fat diet-fed mice) and in vitro (free fatty acid-treated HepG2 cells) in models of NAFLD. We employed RNA-seq and m1A-MeRIP-seq to identify key targets, followed by mechanistic validation of the YTHDF1–m1A–NUPR1 axis using biochemical, histological, and mRNA stability assays.

We identified a critical role for YTHDF1 in promoting hepatic steatosis. NUPR1, a stress-induced transcriptional regulator, undergoes m1A modification. YTHDF1 directly binds to m1A-modified NUPR1 mRNA, enhancing its stability, thereby leading to elevated NUPR1 protein levels. Functionally, upregulated NUPR1 acts as a core driver of NAFLD pathogenesis by activating lipogenic and suppressing fatty acid β-oxidation genes, thereby exacerbating hepatic lipid accumulation.

Our study unveils a novel epitranscriptomic mechanism in which YTHDF1, functioning as a dual-specificity reader, governs NAFLD progression through the m1A-NUPR1 axis. This not only expands the understanding of RNA modification recognition but also establishes the YTHDF1–m1A–NUPR1 pathway as a promising therapeutic target for metabolic liver disease.

Pancreatic solid tumors encompass diverse pathological subtypes. Objective, accurate, and comprehensive imaging examinations and diagnostic reports are essential for preoperative staging, treatment planning, and prognostic evaluation. Currently, China lacks corresponding guidelines or consensus documents, leading to prominent issues including subjective diagnostic reports, incomplete descriptions, and inconsistent terminology. The present guideline was developed to standardize diagnostic imaging reporting of pancreatic solid tumors in China. Relevant domestic and international evidence on imaging examination techniques, key reporting elements, and diagnostic criteria was systematically reviewed and synthesized. This guideline was developed by a multidisciplinary expert panel through systematic evidence retrieval and appraisal, GRADE-based recommendation grading, modified Delphi consensus, and external review. A total of 20 evidence-based recommendations, 13 strong and 7 weak, were formulated, in aspects of imaging examination and diagnostic reporting standards, including the measurement of the tumor size of pancreatic solid tumors, assessment of the obstruction of the main pancreatic duct and common bile duct, definition, assessment, and clinical significance of pancreatic parenchymal atrophy, the assessment of obstructive acute pancreatitis, pseudocysts/retention cysts, and peripancreatic vessels, criteria for resectability, regional lymph node assessment, criteria for suspicious lymph nodes and descriptions of their specific location, and detection of hepatic and peritoneal metastases. Implementation of this guideline in clinical practice will help standardize the accuracy and consistency of diagnostic imaging reports for pancreatic solid tumors in China, thereby advancing standardized imaging diagnosis and informing clinical treatment decisions.

Irinotecan is a camptothecin derivative that exerts its antitumor effects after conversion into the active metabolite 7-ethyl-10-hydroxycamptothecin (SN-38), and it is widely used for the treatment of various advanced solid tumors. However, irinotecan-induced neutropenia (IIN) remains one of its most common and clinically significant hematological toxicities, increasing the risk of infection, treatment interruption, dose reduction, and poor therapeutic outcomes. This review aims to summarize the pathogenesis, risk factors, and management strategies of IIN to provide practical guidance for its clinical prevention and standardized management. Current evidence suggests that IIN is mainly associated with SN-38-mediated topoisomerase I inhibition and mitochondrial injury in hematopoietic stem cells, leading to impaired neutrophil production. The risk of IIN is influenced by irinotecan dosage, UGT1A and transporter gene polymorphisms, baseline patient characteristics, organ function, and concomitant chemotherapy. Preventive and therapeutic strategies include genotype-guided dose adjustment, careful dose optimization, oral alkalinizing agents, granulocyte colony-stimulating factor support, and modulation of intestinal microbiota. In conclusion, IIN is a multifactorial and potentially manageable adverse reaction. Integrating pharmacogenetic testing, individualized dosing, supportive care, and emerging approaches such as microbiota-based interventions may improve the safety and continuity of irinotecan-based chemotherapy.