Tumor immunotherapy has emerged as the fourth major therapeutic modality, following surgery, radiotherapy, and chemotherapy. Unlike traditional treatments that primarily target tumor cells directly, immunotherapy harnesses the body’s immune system to recognize and eliminate cancer cells. Over the past decade, various immunotherapeutic strategies have been developed, including immune checkpoint inhibitors (ICIs), chimeric antigen receptor (CAR) T cell therapy, cancer vaccines, and cytokine-based therapies. However, the immunosuppressive tumor microenvironment (TME) poses a significant obstacle to the effectiveness of these treatments. Polyamines—including putrescine, spermidine, and spermine—are polycationic metabolites that often accumulate abnormally in the TME and act as critical immunoregulatory molecules. T cells play a central role in antitumor immunity, yet their function is frequently influenced by immunoregulatory factors within the TME. Elevated polyamine levels in the TME have been implicated in dampening antitumor T cell responses, thereby facilitating tumor immune evasion. Polyamines in the TME originate from both tumor cells and tumor-associated immune cells. Tumor cells often overexpress the oncogene Myc, which drives the upregulation of polyamine biosynthetic enzymes, resulting in excessive intracellular polyamine production. Additionally, M2-polarized tumor-associated macrophages (M2-TAMs) contribute to polyamine accumulation by upregulating arginase-I (Arg-I), an enzyme that catalyzes the conversion of arginine into ornithine—a key precursor in the polyamine biosynthetic pathway. These combined sources lead to sustained polyamine enrichment in the TME, contributing to immune dysfunction and supporting tumor progression. Moreover, polyamines indirectly affect T cell activity by modulating macrophage polarization and directly suppress tumor cell apoptosis, further promoting an immunosuppressive environment. This review highlights the multifaceted roles of polyamines in modulating tumor-infiltrating T cell function, with a particular focus on their influence on CD4+ T cell differentiation,CD8+ T cell cytotoxicity, and immune checkpoint molecule expression. Recent studies suggest that polyamines suppress CD4+ T cell activation and differentiation by modulating the MAPK/ERK signaling pathway. Additionally, polyamines can impair T cell receptor (TCR) signaling and promote immune evasion through the upregulation of PD-L1 expression on tumor cells. These effects collectively contribute to weakened antitumor T cell responses. Polyamine blocking therapy (PBT), which primarily targets polyamine biosynthesis and transport, has emerged as a novel adjunctive immunotherapeutic strategy in cancer treatment. By reducing polyamine levels in the TME, PBT restores T cell effector functions and alleviates immunosuppression. Notably, studies have demonstrated that combining PBT with ICIs produces synergistic antitumor effects and may overcome resistance to ICI monotherapy. Although research has revealed the inhibitory effects of polyamines on T cell immune function, the underlying regulatory mechanisms remain to be fully elucidated. Moreover, due to compensatory mechanisms employed by tumor cells to maintain polyamine homeostasis, multi-targeted approaches may be necessary to achieve safe and effective therapeutic outcomes. Future PBT strategies may benefit from the integration of multi-omics technologies and the development of nanocarrier-based drug delivery systems, which could collectively enhance their specificity, efficacy, and applicability in cancer immunotherapy. This review systematically elucidates the immunomodulatory effects of polyamines on T cell function within the TME and provides theoretical support and novel insights for the advancement of tumor immunotherapeutic strategies.

Aim To explore the mechanism of action of Guizhi Jia Gegen decoction(GGD)in treating pneu-monia-enteritis induced by H1N1 influenza virus infec-tion in a mouse model,using network pharmacology and molecular docking techniques,followed by in vivo verification.Methods A pneumonia-enteritis mouse model was established,and the intervention effects of GGD on the model mice were evaluated using indica-tors such as body weight,rectal temperature,lung in-dex,colon length,H1N1 M gene expression,relative mRNA expression levels of inflammatory cytokines,and pathological sections of the lung and intestine.The targets of the blood-absorbed components of GGD were identified using the Swiss Target Prediction platform,and the disease targets were retrieved from the Gene-Cards platform.The intersecting targets were analyzed through PPI network analysis using the STRING data-base to identify core targets.GO analysis and KEGG pathway enrichment analysis were performed using the Metascape database.RT-qPCR was employed to vali-date the core targets and pathways.Molecular docking was conducted using AutoDock Tools software to verify the interactions between blood-absorbed components and key targets.Results GGD demonstrated signifi-cant therapeutic effects on the pneumonia-enteritis mouse model.The results of network pharmacology in-dicated that the therapeutic effects of GGD were strong-ly associated with targets such as TNF,ALB,PTGS2,MMP9,EGFR,ESR1,SRC,HSP90AA1,PPARG and MMP2.RT-qPCR results indicated that GGD could intervene in pneumonia-enteritis by regulating the targets TNF,ALB,EGFR and the related targets of the NF-κB pathway.Molecular docking results re-vealed that blood-absorbed components such as puerar-in and liquiritin could stably bind to TNF,ALB and EGFR.Conclusion Components such as puerarin and liquiritin in GGD may exert therapeutic effects on pneumonia-enteritis induced by H1N1 influenza virus infection by acting on targets such as TNF,ALB and EGFR.

Objective To explore the effects of the disinfection port position and diameter and disinfectant concentration on the in-situ decontamination of the flow field-based biosafety high efficiency particulate air filter device with the computational fluid dynamics(CFD)method.Methods ANSYS DesignModeler was used to construct five models for the high efficiency particulate air filter device with the disinfection port at the side end in four ones and upper end in the remained one model,with the diameter being 70,100,150,260 and 260 mm respectively;secondly,a standard k-ε turbulence model was applied to simulating the velocity field and concentration field inside the high efficiency particulate air filter device,so as to analyze the influence of the vortex position inside the device and the structure of the device on the disinfection effect and to determine the optimal structure of the device;finally,H2O2 with the concentration of 0.45,0.35 or 0.30 mol/L was selected as the disinectant to investigate the effect of the disinfectant concentration on the disinfection under the optimal device structure.Results Simulation showed that there were vortexes existed the cavity between the filter compression structure and the filter of the high efficiency particulate air filter device.The disinfection effect in case of the disinfection port at the side end was higher than that in case of the disinfection port at the upper end;the diameter of the disinfection port had influences on the disinfection effect,and high-concentration disinfectant was found in the device when the diameter was 100 mm.The optimal structure with the disinfection port at the side end and the diameter of 100 mm was determined for the high efficiency particulate air filter device.An increase in H2O2 concentration was beneficial to improve disinfection without corroding and damaging the device when the in-situ decontamination of the flow field-based biosafety high efficiency particulate air filter device was carried out.Conclusion The characteristics of the internal flow field of the flow field-based biosafety high efficiency particulate air filter device and the influencing factors of the in-situ disinfection effect are revealed,and theoretical references are provided for the optimal design of the device.[Chinese Medical Equipment Journal,2025,46(9):22-27]

Aim To investigate the association of triglyceride-glucose(TyG)index with microvascular obstruction(MVO)after percutaneous coronary intervention(PCI)in patients with ST-segment elevated myocardial infarction(STEMI).Methods Individual patient-data were pooled from 310 patients with STEMI underwent emergency PCI in Nanjing Drum Tower Hospital,the Affiliated Hospital of Nanjing University Medical School from June 2018 to June 2021 for a prospective analysis.A week following the operation,cardiac magnetic resonance imaging was used to evaluate the MVO region and the patients were divided into two groups based on whether MVO occured after PCI:the MVO group(n=183)and the non-MVO group(n=127).The clinical data of the two groups were compared,and the linear relationship between TyG index and MVO was described using restricted cubic splines(RCS).Univariate and multivariate Logistic regression analysis were used to correct for confounding factors and identify independent risk factors for MVO occurrence.Results After adjustment for confounding factors,TyG index was an independent risk factor for MVO after emergency PCI in STEMI patients,and every 1-unit increased in TyG index,the risk of MVO increased by 1.24 times(OR=2.24,95％CI:1.07～4.71,P=0.033).The RCS curve analysis results showed that there was a linear re-lationship between the TyG index and the occurrence of MVO after emergency PCI(non-linear correlation test P=0.47).When the TyG index was greater than 9.5,the risk of MVO after emergency PCI significantly increased.Conclusion An increased TyG index is postively associated with the incidence of MVO in STEMI patients who have undergone PCI,and has clinical significantce for early prevention and risk stratification of MVO in STEMI patients.

Objective:To investigate the completion rate of tumor evaluation at initial assessment and after neoadjuvant therapy for mid and low rectal cancer patients in the national multicenter real-world database.Methods:The prospective real-world study was conducted. The clinicopathological data of 1 074 patients who underwent surgical treatment for mid and low rectal cancer in 47 national medical institutions, including Peking Union Medical College Hospital et al, from May 12,2023 to May 11,2024 were collected. Observation indicators: (1) clinical characteristics of patients with mid and low rectal cancer; (2) initial colonoscopy and pathologic evaluation of tumors in patients with mid and low rectal cancer; (3) initial imaging evaluation of patients with mid and low rectal cancer; (4) imaging evaluation after neoadjuvant therapy for patients with mid and low rectal cancer. Measurement data with normal distribution were represented as Mean± SD, and measurement data with skewed distribution were represented as M( Q1, Q3). Count data were described as absoluter numbers and/or percentages. Results:(1) Clinical characteristics of patients with mid and low rectal cancer. Of the 1 074 patients, there were 713 males and 361 females, aged 63(56,70)years. The body mass index of 1 074 patients was 24(21,26)kg/m 2.For American Society of Anesthesiologists classification, there were 147 cases of stage Ⅰ, 641 cases of stage Ⅱ, 157 cases of stage Ⅲ, 2 cases of stage Ⅳ, and there were 127 cases missing data. (2) Initial colonoscopy and pathologic evaluation of tumors in patients with mid and low rectal cancer. Of the 1 074 patients, there were 787 cases (73.28%) undergoing complete colonoscopy, and there were only 197 cases (18.34%) undergoing immunohistochemical evaluation of all four mismatch repair proteins. (3) Initial imaging evaluation of patients with mid and low rectal cancer. Of the 1 074 patients, there were 842(78.40%) patients completing magnetic resonance imaging (MRI) or ultrasound evaluation, and there were 914(85.10%) patients completing chest, abdomen, and pelvis enhanced computed tomography (CT) evaluation. In the 149 patients completing rectal ultrasound evaluation, there were 122 cases (81.88%) comple-ting T staging evaluation, and there were 81 cases (54.36%) completing N staging evaluation. In the 808 patients completing rectal MRI evaluation, there were 708 cases (87.62%) completing T staging evaluation, and there were 590 cases (73.02%) completing N staging evaluation. (4) Imaging evalua-tion after neoadjuvant therapy for patients with mid and low rectal cancer. Of the 388 patients with neoadjuvant therapy, there were 332 patients (85.57%) completing MRI or ultrasound evaluation, and there were 327 patients (84.28%) completing chest, abdomen, and pelvis enhanced CT evalua-tion. In the 70 patients completing rectal ultrasound evaluation, there were 65 cases (92.86%) com-pleting T staging evaluation, and there were 49 cases (70.00%) completing N staging evaluation. In the 327 patients completing rectal MRI evaluation, there were 246 cases (75.23%) completing T staging, and there were 228 cases (69.72%) completing N staging evaluation. Conclusion:The com-pletion rate of tumor imaging evaluation at initial assessment and after neoadjuvant therapy for mid and low rectal cancer patients on a national scale is relatively good.

High mobility group box protein 1(HMGB1)is one of the most widely expressed protein member in the HMGs family,which is well known for its involvement in the body inflammatory response.Previous researches have found that it plays a significant role in cell migration,immune identification and neuroprotection.Spinal cord injury is a disease that causes severe damage to the nervous system,and neural circuits are disrupted after a spinal cord injury,which leads to many conditions including ischemia and hypoxia,inflammatory responses,demyelinating lesions,and glial scar formation that are detrimental to nerve regeneration and repair,making it one of the most difficult diseases to treat in the modern spinal surgery field.HMGB1 is upregulated after spinal cord injury,thereby regulating neuroinflam-matory responses,and participating in the neuronal apoptosis,promoting neuronal regeneration,and inducing neural stem cell differentiation and migration,which plays an important role in the process of neural function recovery.This paper summarizes the structure and function of HMGB1,as well as its role in spinal cord injury,in order to provide direction for founding therapeutic target for neurological function recovery after spinal cord injury.

Aim To explore the therapeutic effects of resveratrol(Res)on hepatic inflammation and oxida-tive stress in rheumatoid arthritis(RA),and to eluci-date the relationship of the regulatory mechanism of the Nrf2/Keap1 signaling pathway in it.Methods A mouse model of arthritis was induced using chicken type Ⅱ collagen in combination with complete Freund's adjuvant,and Res was administered by tube feeding for treatment.Serum liver function indices and levels of hepatic inflammation and oxidative stress were detected in mice.An in vitro cellular model of hepatic inflam-mation and oxidative stress was established by treating mouse primary hepatocytes(MPHs)with TNF-α(5μg·L-1),cell proliferation inhibition was detected by CCK-8,and inflammation and oxidative stress-relat-ed indices were detected by protein blotting.The in-trinsic mechanisms by which Res attenuated hepatic in-flammation and oxidative stress in rheumatoid arthritis were explored by treating MPHs with Nrf2 inhibitor and Keap1 overexpression plasmid.Results Res signifi-cantly reduced the levels of inflammation and oxidative stress in hepatic tissues of collagen-induced arthritis mice as well as TNF-α-treated MPHs,and activated the Nrf2/Keap1 signaling pathway.Inflammation and oxidative stress levels in MPHs were exacerbated by the use of Nrf2 inhibitors and Keap1 overexpression,which promoted apoptosis.Conclusion Res attenuates he-patic inflammation and oxidative stress in rheumatoid arthritis via the Nrf2/Keap1 pathway.

Objective:To investigate the predictive value of microRNA-1(miR-1),brain natriuretic peptide(BNP)and ischemia-modified albumin(IMA)for unstable angina pectoris(UAP).Methods:We enrolled 237 UAP patients admitted to Xining Second People's Hospital between June 2018 and December 2020 as UAP group.Another 86 healthy subjects undergoing physical examination simultaneously were enrolled as control group.MiR-1 expression,BNP and IMA levels were measured.General data between UAP group and control group,serum miR-1 expression,BNP and IMA levels among different Braunwald class and prognosis were compared.Receiver operat-ing characteristic(ROC)curve was employed to analyze predictive value of miR-1,BNP,IMA and their combina-tion for prognosis in UAP patients.Results:Compared with participants in the control group,those in UAP group had significant higher serum miR-1 expression[(1.80±0.59)vs.(0.93±0.11)],BNP[(107.34±37.46)pg/ml vs.(52.31±10.64)pg/ml]and IMA[(79.76±19.29)g/L vs.(53.16±6.43)g/L](P＜0.001 all).As Braun-wald class increased(class Ⅰ～Ⅲ),serum miR-1 expression,BNP and IMA levels elevated(P＜0.001 all).Com-pared with patients in favorable outcome group,those in unfavorable outcome group had significant higher serum miR-1 expression[(2.31±0.54)vs.(1.53±0.41)],BNP[(147.03±29.63)pg/ml vs.(85.95±19.46)pg/ml]and IMA[(97.24±15.35)g/L vs.(70.35±13.88)g/L](P＜0.001 all).ROC curve indicated that AUC of com-bined detection for predicting unfavorable outcome in UAP patients was 0.925(95％CI 0.884～0.955),which was significantly higher than miR-1(AUC=0.880,95％CI 0.831～0.918),BNP(AUC=0.863,95％CI 0.813～0.904)and IMA(AUC=0.900,95％CI 0.854～0.935)alone(Z=2.884,3.130,2.090,P＜0.05 or＜0.01).Conclusion:MiR-1 expression,BNP and IMA levels significantly increase in UAP patients,and they are associated with the severity of disease.Combined detection has good predictive value for unfavorable outcome in UAP pa-tients.

High mobility group box protein 1(HMGB1)is one of the most widely expressed protein member in the HMGs family,which is well known for its involvement in the body inflammatory response.Previous researches have found that it plays a significant role in cell migration,immune identification and neuroprotection.Spinal cord injury is a disease that causes severe damage to the nervous system,and neural circuits are disrupted after a spinal cord injury,which leads to many conditions including ischemia and hypoxia,inflammatory responses,demyelinating lesions,and glial scar formation that are detrimental to nerve regeneration and repair,making it one of the most difficult diseases to treat in the modern spinal surgery field.HMGB1 is upregulated after spinal cord injury,thereby regulating neuroinflam-matory responses,and participating in the neuronal apoptosis,promoting neuronal regeneration,and inducing neural stem cell differentiation and migration,which plays an important role in the process of neural function recovery.This paper summarizes the structure and function of HMGB1,as well as its role in spinal cord injury,in order to provide direction for founding therapeutic target for neurological function recovery after spinal cord injury.

Aim To explore the therapeutic effects of resveratrol(Res)on hepatic inflammation and oxida-tive stress in rheumatoid arthritis(RA),and to eluci-date the relationship of the regulatory mechanism of the Nrf2/Keap1 signaling pathway in it.Methods A mouse model of arthritis was induced using chicken type Ⅱ collagen in combination with complete Freund's adjuvant,and Res was administered by tube feeding for treatment.Serum liver function indices and levels of hepatic inflammation and oxidative stress were detected in mice.An in vitro cellular model of hepatic inflam-mation and oxidative stress was established by treating mouse primary hepatocytes(MPHs)with TNF-α(5μg·L-1),cell proliferation inhibition was detected by CCK-8,and inflammation and oxidative stress-relat-ed indices were detected by protein blotting.The in-trinsic mechanisms by which Res attenuated hepatic in-flammation and oxidative stress in rheumatoid arthritis were explored by treating MPHs with Nrf2 inhibitor and Keap1 overexpression plasmid.Results Res signifi-cantly reduced the levels of inflammation and oxidative stress in hepatic tissues of collagen-induced arthritis mice as well as TNF-α-treated MPHs,and activated the Nrf2/Keap1 signaling pathway.Inflammation and oxidative stress levels in MPHs were exacerbated by the use of Nrf2 inhibitors and Keap1 overexpression,which promoted apoptosis.Conclusion Res attenuates he-patic inflammation and oxidative stress in rheumatoid arthritis via the Nrf2/Keap1 pathway.