The crystalline lens of the eye is recognized as one of the most radiosensitive tissues in the human body. While the International Commission on Radiological Protection (ICRP) has classified ionizing radiation (IR)-induced cataracts as a tissue reaction (deterministic effect) and subsequently reduced the occupational equivalent dose limit for the lens, significant uncertainties remain regarding the precise dose threshold and the complex biological pathways driving lens opacification. This review provides a comprehensive synthesis of current knowledge concerning radiation-induced lens damage, integrating epidemiological exposure characteristics with dose-response modeling and mechanistic molecular insights. First, we analyze exposure characteristics through four epidemiological dimensions: dose, time, space, and population. Clinical evidence suggests that radiation cataracts—particularly posterior subcapsular opacities—exhibit a distinct latency period that is inversely correlated with dose. We highlight that risk is not confined to acute high-dose scenarios (such as in atomic bomb survivors) but is increasingly relevant in chronic low-dose occupational settings (e.g., interventional radiology) and medical diagnostics (e.g., CT scans). Crucially, individual susceptibility is modified by genetic background, age, and environmental co-factors, complicating risk assessment. Second, we critically examine the dose-effect relationship. Although the ICRP suggests a threshold of 0.5 Gy, emerging data challenge the traditional threshold model, with some studies advocating for a linear non-threshold (LNT) relationship. We further discuss the critical roles of radiation quality and dose rate. High linear energy transfer (LET) radiation demonstrates a significantly higher relative biological effectiveness (RBE) for cataractogenesis compared to low-LET radiation. Paradoxically, and unlike many other tissues, the lens may exhibit an “inverse dose-rate effect,” where fractionated or protracted exposures potentially enhance biological damage—a finding that challenges classical radiobiological paradigms. Third, drawing upon the “cataractogenic load” hypothesis and the unique physiological constraints of the lens, this review elucidates the multidimensional molecular mechanisms driving radiation-induced opacification. Key mechanisms include four aspects. (1) DNA damage and repair: IR induces DNA double-strand breaks (DSBs) that, due to the lens’ limited repair capacity (modulated by genes such as ATM, Ptch1, and Ercc2), lead to the accumulation of damage. (2) Antioxidant defense system: dysfunction of the Nrf2/HO-1 antioxidant axis results in redox imbalances, triggering NF-κB-mediated inflammation and protein aggregation. (3) Cell proliferation and senescence: IR disrupts cell cycle regulation, causing a dichotomy of effects—driving premature senescence in some cell populations (evidenced by ATM nuclear foci) while inducing aberrant proliferation via growth factor upregulation (FGF2, TGFβ) in others. (4) Cell migration and adhesion: activation of the Wnt/β‑catenin pathway and alterations in the E-cadherin complex promote the abnormal migration of epithelial cells to the posterior capsule, a hallmark of radiation-induced cataracts. In conclusion, radiation-induced cataractogenesis is a multifactorial process in which genetic susceptibility and environmental stressors converge to overwhelm the lens’ homeostatic thresholds. Future research must prioritize longitudinal cohort studies to refine dose thresholds and employ multi-omics approaches to map the crosstalk between DNA damage responses and matrix remodeling. Establishing a robust mechanistic model is essential for developing targeted radioprotective strategies and optimizing radiation protection standards for occupational and medical safety.

OBJECTIVE To explore the mechanism of Yishen Qingli Huoxue Formula(YQHF)improving renal fibrosis by inhib-iting HIF1-α using data mining,molecular docking,and in vivo and in vitro experiments.METHODS The expression changes of HIF1-α in renal biopsy tissues of patients with chronic kidney disease(CKD)in the GEO database were analyzed.Molecular docking was used to clarify the interaction mode between YQHF effective monomers and HIF1-α.Thirty SD rats were randomized to sham,model,low-dose YQHF,high-dose YQHF,and losartan potassium groups(n=6 per group).Unilateral ureteral obstruction(UUO)was used to induce renal fibrosis.Serum creatinine(Scr)and blood urea nitrogen(BUN)were measured,and kidney sections were stained with HE and Masson to assess pathology and fibrosis.Renal HIF1-α protein expression was quantified by Western blot.A renal fibro-sis cell model was established by inducing NRK-52E cells with TGF-β1,and the cells were divided into control,model,YQHF,HIF1-α inhibitor,HIF1-α inhibitor+YQHF,HIF1-α agonist,and HIF1-α agonist+YQHF groups.Western blot analysis was used to detect the protein expression levels of HIF1-α,COL-1,and α-SMA,and to observe the mechanism of YQHF-containing serum in protecting renal tubular epithelial cells.RESULTS Data mining showed HIF1-α expression in the CKD group was significantly higher than in the control group(P<0.01).Molecular docking indicated YQHF core components had good binding affinity to HIF1-α.In vivo,com-pared with the sham group,HE staining revealed tubular atrophy and inflammatory-cell infiltration,and Masson staining showed in-creased collagen deposition in UUO model rats(P<0.01).Serum creatinine and blood urea nitrogen were also elevated in the model group(P<0.05),together with up-regulated renal expression of COL-1,α-SMA and HIF-1α(P<0.01).After intervention with either high-dose or low-dose YQHF or losartan potassium,these pathological changes were attenuated:collagen deposition decreased(P<0.01),creatinine and BUN fell to varying degrees(P<0.05),and renal COL-1,α-SMA and HIF-1α levels were down-regulated(P<0.01);immunohistochemistry confirmed reduced HIF-1α in UUO kidneys(P<0.01).In NRK-52E cells,TGF-β1 stimulation mark-edly increased COL-1,α-SMA and HIF-1α protein levels(P<0.01).Both YQHF and chloramphenicol alone down-regulated these proteins(P<0.05,P<0.01),and their combination produced stronger inhibition of HIF-1α than YQHF alone(P<0.05).Conversely,the HIF-1α agonist fenbendazole-d3 reversed YQHF's anti-fibrotic effect,re-elevating COL-1,α-SMA and HIF-1α(P<0.01),with no significant difference versus agonist alone.CONCLUSION YQHF may inhibit extracellular matrix deposition and delay renal fi-brosis progression by suppressing HIF1-α accumulation,providing new theoretical evidence for traditional Chinese medicine in treat-ing renal fibrosis.

Objective To develop a portable heat illness/stroke first-aid kit for on-site first aid of heat illness patients and verify its application effect.Methods The portable heat illness/stroke first-aid kit was composed of a main box,an adjustable telescopic rod,adjustable shoulder straps,universal rollers and a thermal insulation container.The main box made of aluminum alloy material had the inner surface lined with Oxford cloth,which was equipped with an infrared cochlear thermometer,a nebulizer,first aid medicines,heat stroke medicines,a sun umbrella,a cooling blanket,etc;the adjustable telescopic rod was made of aluminum-magnesium alloy;the adjustable shoulder straps was made of high-density nylon webbing;the universal rollers were rubberized and had wheel brakes;the thermal insulation container was located in the lower storage compartment inside the main box,which used polyurethane(PU)material for thermal insulation.The data on on-site first aid of the patients with moderate heat illness or stroke at some institution from 2019 to 2022 were analyzed retrospectively,with the patients treated with the traditional methods enrolled into a control group and the ones with the first-aid kit into an experimental group.The temperature changes at 0,10,20,30,40,50 and 60 min after the start of treatment were investigated to compare the cooling effects of the two groups.Results The heat illness/stroke first-aid kit lowered the patient temperature effectively during the on-site first aid of the patients with moderate heat illness or stroke,with higher cooling speed and effect than the traditional methods,especially at the early stage of treatment.Conclusion The heat illness/stroke first-aid kit with complete functions and easy operation decreases temperature of heat illness patients efficiently,and can be applicable to the scenarios such as field training and outdoors high-temperature operation.[Chinese Medical Equipment Journal,2025,46(9):108-113]

Objective:To evaluate the effect of low-dose esketamine on intraoperative electroencephalogram (EEG) burst suppression under general anesthesia in elderly patients.Methods:In this prospective randomized controlled trial, 86 elderly patients of either sex, scheduled for elective lumbar fusion surgery at Anhui No. 2 Provincial People′s Hospital from March 15 to June 1, 2024, aged 60-85 yr, with a body mass index of 18-28 kg/m 2, of American Society of Anesthesiologists Physical Status classification ⅡorⅢ, were divided into 2 groups ( n=43 each) using a random number table method: esketamine group (group S) and control group (group C). In group S, esketamine at a dose of 0.25 mg/kg was intravenously injected after anesthesia induction, while the equal volume of normal saline was intravenously injected in group C. The occurrence of EEG burst suppression and frequency of the characteristic density spectral array were recorded using the Masimo Sedline cerebral function monitor. The patient state index was recorded before esketamine administration and at 5, 10, 30 and 60 min after administration and at 5 min before the end of the surgery. Delirium was assessed using the Confusion Assessment Method at 1 and 3 days after operation. The total pressing times of patient-controlled analgesia within 48 h after operation, requirement for rescue analgesia and occurrence of adverse reactions (nausea and vomiting, delayed emergence from anesthesia, agitation, headache) were recorded. The consumption of ephedrine, phenylephrine, sufentanil and remifentanil during operation, emergence time, time of tracheal extubation, length of stay in the post-anesthesia care unit, and length of postoperative hospital stay were also recorded. Results:Compared with group C, the incidence of EEG burst suppression and frequency of the characteristic density spectral array were significantly decreased, the patient state index values were increased at each time point after administration and 5 min before the end of surgery, the consumption of ephedrine, phenylephrine, sufentanil and remifentanil during operation was reduced, the effective pressing times of patient-controlled analgesia, rate of rescue analgesia, and incidence of postoperative delirium within 3 days after operation were decreased, and the length of postoperative hospital stay was shortened in group S ( P<0.05). Conclusions:Low-dose esketamine can reduce intraoperative EEG burst suppression and decrease the development of postoperative delirium under general anesthesia in elderly patients.

Objective To investigate the effect and mechanism of long non-coding RNA(lncRNA)NRON on myocardial fibrosis in mice with myocardial infarction(MI).Methods Thirty-two C57/BL6 mice were randomly assigned to a Sham group,MI group,MI+shNRON group or MI+NC group,with eight mice in each group.The expression level of lncRNA NRON in myocardial tissue of mice was detected by real-time quantitative PCR.Hematoxylin and eosin staining,Masson's trichrome staining,and immunohistochemistry were used to detect the degree of myocardial injury,myocardial fibrosis,and the expression level of collagen Type Ⅰ(col Ⅰ).Western blotting was used to detect the protein expression levels of TGF-β1,p-Smad2,and p-Smad3 in myocardial tissue of the mice.Results Compared with the Sham group,the expression of NRON,col Ⅰ,TGF-β1,p-Smad2,and p-Smad3 proteins were increased in the MI group.Compared with the MI group,the expression of NRON,the degree of myocardial damage and fibrosis,the expression of col Ⅰ,TGF-β1,p-Smad2,and p-Smad3 proteins were decreased in the MI+shNRON group.Conclusion Down-regulation of lncRNA NRON can alleviate myocardial injury and inhibit myocardial fibrosis in mice with MI,and the molecular mechanism may be related to inhibition of the TGF-β/Smad signaling pathway.

Objective:To explore the effect and mechanism of CD147 on differentiation of circulating fibrocytes and its pro-inflammatory and pro-fibrotic function.Methods:Circulating fibrocytes were extracted from peripheral blood of asthma patients,stimu-lated with CD147,and intervened with CD147 antagonist AP-9 or p38/MAPK inhibitor SB203580.Cell viability was detected by CCK-8 method,cell migration was assessed by Transwell method,expressions of collagen type Ⅰ(COL-Ⅰ),CD45 and α-SMA were detected by immunofluorescence staining.Levels of cytokines such as TGF-β1,IL-4,IL-5 and IL-13 were detected by ELISA,and expression levels of COL-Ⅰ,fibronectin(FN),α-SMA,p-TAK1,p-P38 and other proteins were detected by Western blot.Results:Low dose of CD147 increased cell viability of circulating fibrocytes.CD147 significantly promoted migration of circulating fibrocytes and induces their differentiation into myofibrocytes.CD147 significantly increased secretion of cytokines such as TGF-β1,IL-4,IL-5 and IL-13 in circulating fibrocytes.CD147 significantly increased expressions of COL-Ⅰ,FN,α-SMA,p-TAK1,p-P38 in circulating fibrocytes.AP-9 or SB203580 significantly inhibited effect of CD147 on circulating fibrocytes.Conclusion:CD147 can promote proliferation,mi-gration,differentiation and pro-inflammatory and profibrotic function of circulating fibrocytes in vitro,and TAK1-p38/MAPK signaling pathway is involved in CD147-mediated regulation of circulating fibrocytes.

Objective To investigate the effect and mechanism of long non-coding RNA(lncRNA)NRON on myocardial fibrosis in mice with myocardial infarction(MI).Methods Thirty-two C57/BL6 mice were randomly assigned to a Sham group,MI group,MI+shNRON group or MI+NC group,with eight mice in each group.The expression level of lncRNA NRON in myocardial tissue of mice was detected by real-time quantitative PCR.Hematoxylin and eosin staining,Masson's trichrome staining,and immunohistochemistry were used to detect the degree of myocardial injury,myocardial fibrosis,and the expression level of collagen Type Ⅰ(col Ⅰ).Western blotting was used to detect the protein expression levels of TGF-β1,p-Smad2,and p-Smad3 in myocardial tissue of the mice.Results Compared with the Sham group,the expression of NRON,col Ⅰ,TGF-β1,p-Smad2,and p-Smad3 proteins were increased in the MI group.Compared with the MI group,the expression of NRON,the degree of myocardial damage and fibrosis,the expression of col Ⅰ,TGF-β1,p-Smad2,and p-Smad3 proteins were decreased in the MI+shNRON group.Conclusion Down-regulation of lncRNA NRON can alleviate myocardial injury and inhibit myocardial fibrosis in mice with MI,and the molecular mechanism may be related to inhibition of the TGF-β/Smad signaling pathway.

To achieve efficient and rapid detection of duck astrovirus type 2(DAstV-2),RPA prim-ers and crRNA were designed and synthesized based on the conserved sequence of the ORF2 gene of DAstV-2.A detection method for DAstV-2 was constructed,integrating RPA nucleic acid ampli-fication,LwCas13a cleavage,and colloidal gold lateral flow dipstick visualization.The specificity,sensitivity,and concordance of this detection method were evaluated.The experimental results showed that the detection limit for the DAstV-2 recombinant plasmid standard was 1.2×101 cop-ies/μL,which is superior to the conventional RT-PCR method.The method can specifically detect DAstV-2 pathogenic nucleic acids without cross-reactivity with DAstV-1,DAstV-3,DAstV-4,duck plague virus(DEV),and duck tembusu virus(DTMUV).When testing liver tissue samples from ducks suspected of being infected with DAstV-2,the results obtained using this method were com-pletely consistent with those from real-time quantitative PCR,with a 100％concordance rate.How-ever,this method is simpler and faster to perform.The research indicates that the established RPA-CRISPR/Cas13a-LFD detection system has high sensitivity,strong specificity,and high accuracy,capable of completing rapid visual detection of DAstV-2 nucleic acids within 1 h at a constant tem-perature of 37 ℃,providing a new technical platform for the rapid diagnosis of DAstV-2.

Objective:To explore the effect and mechanism of CD147 on differentiation of circulating fibrocytes and its pro-inflammatory and pro-fibrotic function.Methods:Circulating fibrocytes were extracted from peripheral blood of asthma patients,stimu-lated with CD147,and intervened with CD147 antagonist AP-9 or p38/MAPK inhibitor SB203580.Cell viability was detected by CCK-8 method,cell migration was assessed by Transwell method,expressions of collagen type Ⅰ(COL-Ⅰ),CD45 and α-SMA were detected by immunofluorescence staining.Levels of cytokines such as TGF-β1,IL-4,IL-5 and IL-13 were detected by ELISA,and expression levels of COL-Ⅰ,fibronectin(FN),α-SMA,p-TAK1,p-P38 and other proteins were detected by Western blot.Results:Low dose of CD147 increased cell viability of circulating fibrocytes.CD147 significantly promoted migration of circulating fibrocytes and induces their differentiation into myofibrocytes.CD147 significantly increased secretion of cytokines such as TGF-β1,IL-4,IL-5 and IL-13 in circulating fibrocytes.CD147 significantly increased expressions of COL-Ⅰ,FN,α-SMA,p-TAK1,p-P38 in circulating fibrocytes.AP-9 or SB203580 significantly inhibited effect of CD147 on circulating fibrocytes.Conclusion:CD147 can promote proliferation,mi-gration,differentiation and pro-inflammatory and profibrotic function of circulating fibrocytes in vitro,and TAK1-p38/MAPK signaling pathway is involved in CD147-mediated regulation of circulating fibrocytes.

Objective To design a combat rescue specialized physical training simulator to solve the problems of the existing combat rescue physical traing in multifunctionality and simulation vividness.Methods The simulator was divided into three types for stretcher handling,land combat rescue and marine rescue based on the application scenerio and functional positioning,and into three grades of basic level,intensive level and ultra intensive level based on the loaded mass and additional weight object.The main components of the simulator included a manikin,a bionic joint and addtional weight objects.The manikin was made up of outer skin,inner liner and skeleton;the bionic joint was made of stainless steel with surface electrophoresis treatment,and was composed of high-strength medal bearing shafts with multiple disc springs and damping mechanisms;the additional weight objects involued in high-intensity cast iron or lead blocks,which were pre-embedded,mounted or srtapped into the simulator.The simulator was verified with body shape and mass detection,drop test,waterproof test and drag test.Results It's proved the simulator gained advantages in vividness for body shape and mass,bionic joint structure and adaptability to training environments and could be used for graded physical training in typical combat rescue scenerios.Conclusion The simulator developed solves the problems of the combat rescue specialized physical training equipment,and facilitates the enhancement of physical training of combat rescue personnel.[Chinese Medical Equipment Journal,2025,46(1):33-37]