Cirrhotic portal hypertension is a clinical syndrome caused by persistently elevated portal venous pressure due to liver cirrhosis and can lead to a series of complications， among which esophagogastric variceal bleeding has become one of the most severe complications due to sudden onset and a high mortality rate. Since the release of Expert consensus on diagnosis and treatment of esophagogastric variceal bleeding in cirrhotic portal hypertension （2019 edition）， significant advances have been achieved in this field in China and globally. In order to formulate an expert consensus aligned with the situation of China， Chinese Society of Surgery， Chinese Medical Association organized and compiled Expert Consensus on diagnosis and treatment of esophagogastric variceal bleeding in cirrhotic portal hypertension （2025 edition）. This article elaborates on the key updates in the new edition and explores the major differences between the old and new editions， in order to enhance the understanding of the new edition among clinicians and provide a reference for clinicians in clinical work.

Cutibacterium avidum(C.avidum)is a Gram-positive bacterium belonging to Corynebacterium cutis,which mainly exists on the surface of human skin and rarely causes invasive infection of superficial or deep skin.At present,there is no unified expert consensus on the diagnosis,treatment and prognosis of C.avidum.This paper reports a patient with epidermoid cyst caused by C.avidum who recovered and was discharged after neurosurgical resection of superficial mass and antimicrobial treatment,aiming to enhance the clinical recognition on C.avidum infection and provide reference for the diagnosis and treatment of the disease.

Objective To investigate the effect and mechanism of melatonin in alleviating hypoxia-induced apoptosis in ovarian gra-nulosa cells.Methods Rat ovarian granulosa cells were isolated and divided into normoxic,hypoxic,and melatonin groups.Hypoxia-induced injury models were established in the hypoxic and melatonin groups,and granulosa cells in the melatonin group were treated with melatonin.A total of 24 rats were randomized into the control,model,and intervention groups(n=8 per group).Rat models of declining ovarian function induced by long-term hypoxia were established in the model and intervention groups.The rats in the intervention group were intraperitoneally injected with melatonin.Cell proliferation was measured using a CCK-8 assay,and lactate secretion and HIF-1αprotein with a specific kit,respectively.The levels of estradiol and progesterone in the cell supernatant and rat serum were detected using ELISA.Granulosa cell apoptosis was detected by flow cytometry,ovarian morphology by HE staining,and Bax and caspase-3 expression by Western blotting.Results Compared with the normoxic group,the hypoxic group exhibited decreased granulosa cell proliferation,increased apoptosis,elevated lactate and HIF-1α levels,and reduced estradiol and progesterone levels(P＜0.05).Compared with hypoxic group,these changes were significantly reversed in the molatonin group(P＜0.05).Compared with the control group,the model group showed increased lactate,HIF-1α,Bax,and caspase-3 levels,decreased estradiol and progesterone levels,and reduced follicles.Compared with the model group,all the indicators were ameliorated in the intervention group(P＜0.05).Conclusion Melatonin alleviated hypoxia-induced granulosa cell apoptosis and promoted the recovery of ovarian function.

Objective:To understand the current status, research hotspots, and future trends in the field of retinoblastoma (RB).Methods:Using the Web of Science Core Collection SSCI and SCI-Expanded as data sources, relevant RB literature from January 2015 to November 2024 was retrieved. The bibliometric analysis software CiteSpace 6.2.R6 was employed to perform visual analyses of countries/regions, institutions, journals, authors, co-cited references, and keywords.Results:A total of 5 042 relevant publications were identified. Annual publication numbers in this field consistently exceeded 400, peaking at 565 in 2021. The United States contributed the highest number of publications, with 1 600 articles (31.73%). Among institutions, Harvard University ranked first with 167 publications (3.31%). Abramson DH of Memorial Sloan Kettering Cancer Center published the most papers (75). Nature (United Kingdom) received the highest citation count (2 349). The highest betweenness centrality was observed for the United States (0.14) among countries/regions, Shanghai Jiao Tong University (0.21) among institutions, and Berry JL of Children’s Hospital Los Angeles (0.21) at the author level. Co-citation and keyword analyses revealed that RB research hotspots are shifting from a focus on basic molecular mechanisms, such as the cell cycle and RB protein, toward advanced therapeutic strategies, such as intra-arterial chemotherapy and nanoparticle-based drug delivery. Emerging keywords such as complexity, chemoresistance and carboplatin indicate that future studies will focus on optimising diagnosis and treatment. Conclusions:From 2015 to 2024, RB research displayed a sustained growth trend, with the United States and its institutions and scholars contributing the most publications. The research focus has shifted from the exploration of molecular mechanisms to the optimization of precise treatment strategies, among which the application of nanotechnology and the resolution of drug resistance mechanisms will become key breakthrough directions.

Fundus neovascularization is a significant cause of ocular diseases, mainly including retinal neovascularization and choroidal neovascularization. Anti-vascular endothelial growth factor therapy, though effective, has limitations such as a short half-life, non-responsiveness, and drug resistance. 6-Phosphofructo-2-kinase/fructose-2,6-bisphosphatase 3 (PFKFB3), a key regulator of glycolysis, affects the generation of pathological blood vessels by modulating the metabolism of vascular endothelial cells. Small molecule inhibitors targeting PFKFB3 protein have been confirmed in animal and cell models to significantly inhibit pathological angiogenesis, showing good therapeutic potential. However, most of them are still in the preclinical research stage. In the future, it is necessary to further investigate the mechanism of PFKFB3 gene, optimize the specificity and safety of the inhibitors, and explore the effects of combining them with existing therapies, so as to provide new strategies for the treatment of fundus neovascular diseases.

Aortic dissection(AD)is a life-threatening acute vascular disease with a complex and not yet fully un-derstood pathogenesis.In recent years,metabolic reprogramming has gradually emerged as a significant factor in the oc-currence and development of AD.This review summarizes the abnormal alterations in major metabolic pathways,including amino acid metabolism,glucose metabolism,and lipid metabolism,and their impact on vascular cell functions in AD.Metabolic reprogramming contributes to the progression of AD by regulating the functions of endothelial cells(EC)and vascular smooth muscle cells(VSMC),thereby promoting the destruction of the vascular wall structure and exacerba-ting inflammatory responses.Additionally,this paper summarizes the potential applications of metabolism-related mole-cules in the early diagnosis and treatment of AD,emphasizing the importance of metabolic regulation as a novel strategy for AD prevention and management.Finally,future research directions in the study of metabolic reprogramming in AD are proposed,including in-depth mechanistic studies,the development of novel biomarkers,and the optimization of clinical in-tervention strategies,aiming to provide new insights and methods for the prevention and treatment of AD.

Cutibacterium avidum(C.avidum)is a Gram-positive bacterium belonging to Corynebacterium cutis,which mainly exists on the surface of human skin and rarely causes invasive infection of superficial or deep skin.At present,there is no unified expert consensus on the diagnosis,treatment and prognosis of C.avidum.This paper reports a patient with epidermoid cyst caused by C.avidum who recovered and was discharged after neurosurgical resection of superficial mass and antimicrobial treatment,aiming to enhance the clinical recognition on C.avidum infection and provide reference for the diagnosis and treatment of the disease.

Objective:To construct a calcium alginate (ALG-Ca 2+) composite hydrogel loaded with chlorella protein (Cp) (ALG-Ca 2+@Cp) and investigate its combined effect with microwave hyperthermia on the proliferation, apoptosis, and immune activation of mouse pancreatic cancer cells. Methods:ALG-Ca 2+@Cp was prepared using a physical cross-linking method and its physiochemical properties was characterized via scanning electron microscopy, rheological analysis, Ca 2+ release experiments, and microwave thermal conversion tests. The BCA protein quantification assay was used to evaluate the adsorption capacity of ALG-Ca 2+@Cp for pancreatic cancer cell antigens. The effects of ALG-Ca 2+@Cp extract combined with microwave intervention on pancreatic cancer cell proliferation, apoptosis protein expression, and cell viability were assessed using CCK-8 assays, ELISA, and Calcein-AM/PI double fluorescence staining. Flow cytometry was performed to determine the maturation-promoting ability of ALG-Ca 2+@Cp on immature mouse bone marrow-derived dendritic cells (BMDCs). Results:ALG-Ca 2+@Cp exhibited a three-dimensional network structure with a storage modulus (G') greater than the loss modulus (G''), demonstrating typical hydrogel properties. The hydrogel loaded with 0.5 mol/ml Ca 2+ reached 48°C after 5 minutes of microwave irradiation at 5.0 W/cm 2, and Ca 2+ release plateaued within 5 minutes. ALG-Ca 2+@Cp effectively adsorbed pancreatic cancer cell antigens. Combined with microwave treatment, it significantly reduced pancreatic cancer cell proliferation ( A450 value 0.39±0.07 vs 2.78±0.15) and increased apoptosis markers calreticulin (CRT) and high mobility group box-1 protein (HMGB1) [(557.09±37.84) pg/ml vs (135.14±11.84) pg/ml, (4.77±0.18) ng/ml vs (1.6±0.16) ng/ml], leading to decreased cell viability; and all the differences were statistically significant (all P value <0.05). ALG-Ca 2+@Cp synergistically promoted the maturation of immature BMDCs in the presence of pancreatic cancer antigens, with a CD 80+ positivity rate of (75.67±6.53)%. Conclusions:ALG-Ca 2+@Cp is successfully constructed. Its combination with microwave hyperthermia can significantly enhance the cytotoxicity and immune activation against mouse pancreatic cancer cells by targeting intracellular antigens and inducing immunogenic cell death.

Aortic dissection(AD)is a life-threatening acute vascular disease with a complex and not yet fully un-derstood pathogenesis.In recent years,metabolic reprogramming has gradually emerged as a significant factor in the oc-currence and development of AD.This review summarizes the abnormal alterations in major metabolic pathways,including amino acid metabolism,glucose metabolism,and lipid metabolism,and their impact on vascular cell functions in AD.Metabolic reprogramming contributes to the progression of AD by regulating the functions of endothelial cells(EC)and vascular smooth muscle cells(VSMC),thereby promoting the destruction of the vascular wall structure and exacerba-ting inflammatory responses.Additionally,this paper summarizes the potential applications of metabolism-related mole-cules in the early diagnosis and treatment of AD,emphasizing the importance of metabolic regulation as a novel strategy for AD prevention and management.Finally,future research directions in the study of metabolic reprogramming in AD are proposed,including in-depth mechanistic studies,the development of novel biomarkers,and the optimization of clinical in-tervention strategies,aiming to provide new insights and methods for the prevention and treatment of AD.

Objective:To construct a calcium alginate (ALG-Ca 2+) composite hydrogel loaded with chlorella protein (Cp) (ALG-Ca 2+@Cp) and investigate its combined effect with microwave hyperthermia on the proliferation, apoptosis, and immune activation of mouse pancreatic cancer cells. Methods:ALG-Ca 2+@Cp was prepared using a physical cross-linking method and its physiochemical properties was characterized via scanning electron microscopy, rheological analysis, Ca 2+ release experiments, and microwave thermal conversion tests. The BCA protein quantification assay was used to evaluate the adsorption capacity of ALG-Ca 2+@Cp for pancreatic cancer cell antigens. The effects of ALG-Ca 2+@Cp extract combined with microwave intervention on pancreatic cancer cell proliferation, apoptosis protein expression, and cell viability were assessed using CCK-8 assays, ELISA, and Calcein-AM/PI double fluorescence staining. Flow cytometry was performed to determine the maturation-promoting ability of ALG-Ca 2+@Cp on immature mouse bone marrow-derived dendritic cells (BMDCs). Results:ALG-Ca 2+@Cp exhibited a three-dimensional network structure with a storage modulus (G') greater than the loss modulus (G''), demonstrating typical hydrogel properties. The hydrogel loaded with 0.5 mol/ml Ca 2+ reached 48°C after 5 minutes of microwave irradiation at 5.0 W/cm 2, and Ca 2+ release plateaued within 5 minutes. ALG-Ca 2+@Cp effectively adsorbed pancreatic cancer cell antigens. Combined with microwave treatment, it significantly reduced pancreatic cancer cell proliferation ( A450 value 0.39±0.07 vs 2.78±0.15) and increased apoptosis markers calreticulin (CRT) and high mobility group box-1 protein (HMGB1) [(557.09±37.84) pg/ml vs (135.14±11.84) pg/ml, (4.77±0.18) ng/ml vs (1.6±0.16) ng/ml], leading to decreased cell viability; and all the differences were statistically significant (all P value <0.05). ALG-Ca 2+@Cp synergistically promoted the maturation of immature BMDCs in the presence of pancreatic cancer antigens, with a CD 80+ positivity rate of (75.67±6.53)%. Conclusions:ALG-Ca 2+@Cp is successfully constructed. Its combination with microwave hyperthermia can significantly enhance the cytotoxicity and immune activation against mouse pancreatic cancer cells by targeting intracellular antigens and inducing immunogenic cell death.