OBJECTIVE To upgrade and perfect the quality standard of Psidii Guajavae Folium. METHODS A total of 24 batches of Psidii Guajavae Folium samples were adopted in this study. The macroscopic traits and powder microscopic features of the medicinal materials were observed， and thin-layer chromatography （TLC） identification was carried out. In accordance with corresponding methods documented in Volume Ⅳ of the 2025 edition of the Chinese Pharmacopoeia， multiple indexes were determined， including foreign matter， moisture， total ash， acid-insoluble ash， water-soluble extractives， heavy metals （lead， cadmium， copper， arsenic， mercury） as well as residues of 47 prohibited pesticides. A high-performance liquid chromatography （HPLC） method was established to quantify guaijaverin in Psidii Guajavae Folium. Meanwhile， the HPLC fingerprint of the herb was constructed， followed by similarity evaluation and cluster analysis of all samples. RESULTS The macroscopic traits of Psidii Guajavae Folium complied with relevant specifications of quality standards. Distinct microscopic characteristics were observed in medicinal powder， including non-glandular hairs， calcium oxalate crystals， vessels and stomata. TLC results revealed identical fluorescent spots at positions corresponding to the guaijaverin reference substance on chromatograms of test samples. Among the 24 batches of samples， the detection ranges were 0.3%-2.8% for foreign matter， 5.1%-10.7% for moisture， 5.3%-7.2% for total ash， 0.4%-1.8% for acid-insoluble ash， and 11.8%-26.3% for water-soluble extractives. The test results of heavy metals， harmful elements and prohibited pesticide residues all satisfied the Chinese Pharmacopoeia limit criteria. Methodological validation of content determination and fingerprint analysis met relevant validation requirements. The guaijaverin content of the 24 batches ranged from 0.14% to 0.28%. The HPLC fingerprint similarity values of all samples fluctuated between 0.828 and 0.997； fifteen common peaks were calibrated， six of which were chemically identified. The 24 batches were divided into two major clusters， and cluster classification showed high consistency with sample origins. CONCLUSIONS This research optimizes the TLC identification protocol of Psidii Guajavae Folium and supplements new quality control items including quantitative assay and chromatographic fingerprint. Tentative quality limits are proposed as follows： moisture ≤12.0%， total ash ≤8.0%， water-soluble extractives ≥10.0%， and guaijaverin content ≥0.14% （calculated based on dry products）.

OBJECTIVE To compare the short-term efficacy and safety of small-caliber polyvinyl alcohol （PVA） microsphere-based transcatheter arterial chemoembolization （TACE） versus conventional iodized oil emulsion-based TACE in the treatment of unresectable hepatocellular carcinoma （HCC）.METHODS Clinical data of 146 patients with unresectable HCC who underwent TACE at Gansu Provincial Second People’s Hospital （Affiliated Hospital of Northwest Minzu University） from June 1， 2024， to June 30， 2025， were retrospectively collected. According to the treatment strategy， the patients were divided into the control group （conventional iodized oil emulsion-based TACE， n ＝79） and the observation group （small-caliber PVA microsphere-based TACE， n ＝67）. One-to-one propensity score matching （PSM） was performed， and the matched cohort （62 patients in each group） was used for the primary analysis. The objective response rate （ORR） and disease control rate （DCR） at 1 and 3 months post-treatment， serum levels of tumor markers （alpha-fetoprotein， alpha-fetoprotein lectin-binding fraction L3， and protein induced by vitamin K absence or antagonist-Ⅱ） before treatment and at 1 and 3 months post-treatment， the occurrence of adverse events， progression-free survival （PFS）， and overall survival （OS） were compared between the two groups. Sensitivity and interaction analyses were also performed.RESULTS After PSM， the ORRs in the observation group at 1 and 3 months post-treatment were both 59.7%， and the DCRs were 91.9% and 93.5%， respectively， significantly higher than those in the control group （ORRs： 41.9% and 38.7%； DCRs： 77.4% and 75.8%； P ＜0.05）. At 1 and 3 months post-treatment， the serum levels of tumor markers decreased significantly from baseline in both groups， with significantly lower levels in the observation group than in the control group （ P ＜0.05）. No statistically significant differences were observed in the overall incidence of adverse events or the incidence of grade≥3 adverse events between the two groups （ P ＞0.05）. The median PFS was 10.6 months in the control group and 14.3 months in the observation group， with no statistically significant difference [hazard ratio （HR） of 0.69， 95% confidence interval （CI） of 0.44-1.09， P ＝0.111]. During follow-up， 8 and 9 patients died in the control and observation groups， respectively， and the median OS was not reached in either group. The 12-month OS rates were 88.8% and 87.3%， respectively， with no statistically significant difference （HR of 0.88， 95%CI of 0.35-2.24， P ＝0.790）. After adjustment for potential confounding factors in the original cohort， the ORR at 3 months post-treatment remained significantly higher in the observation group than in the control group （adjusted odds ratio of 2.67， 95%CI of 1.28-5.56， P ＝0.009）. Additionally， the interaction between treatment modality and Barcelona Clinic Liver Cancer staging had no statistically significant impact on the ORR at 3 months post-treatment （ P ＝0.391）.CONCLUSIONS For patients with unresectable HCC， compared with conventional iodized oil emulsion-based TACE， small-caliber PVA microsphere-based TACE demonstrates superior efficacy in terms of early radiological response and improvement in tumor markers， and the two regimens are comparable in terms of safety.

BACKGROUND:In the skeleton,various endogenous or exogenous stimuli cause imbalance in bone metabolism,leading to changes in bone mass and bone strength,which in turn cause a series of bone-related diseases such as osteoarthritis and osteoporosis.In this process,Forkhead box transcription factor O1(FoxO1)plays an important role,and FoxO1 can regulate bone metabolism by regulating oxidative stress,cell proliferation,differentiation and apoptosis. OBJECTIVE:This paper focuses on FoxO1,and by summarizing its upstream and downstream regulatory mechanisms,it provides new ideas for the future treatment of bone-related diseases. METHODS:The search terms"FoxO1,Bone"were used for literature retrieval in CNKI and WanFang Databases,and the search terms"FoxO1,Bone,Skeleton"were used in PubMed and Web of Science databases.The old,repetitive,poor quality and irrelevant papers were excluded,and 56 papers were finally included for review and analysis. RESULTS AND CONCLUSION:(1)FoxO1 promotes the differentiation of bone marrow mesenchymal stem cells into osteoblasts by increasing the expression of runt-related transcription factor 2,alkaline phosphatase and osteocalcin,and transforms bone marrow mesenchymal stem cells from lipogenic differentiation to osteogenic differentiation by inhibiting peroxisome proliferator-activated receptor γ,thereby increasing bone formation.In addition,FoxO1 may also affect bone formation by increasing the number of osteoblasts.(2)Inhibition of FoxO1 in bone marrow mononuclear macrophages can reduce the expression of macrophage colony-stimulating factor,receptor activator of nuclear factor-κB ligand and nuclear factor of activated T cells 1,promote the expression of FoxO1 in osteoclasts,and thus inhibit osteoclast differentiation.In addition,direct activation of FoxO1 also inhibits osteoclast differentiation and weakens osteoclast activity.(3)Upregulation of FoxO1 in chondrocytes can regulate chondrocyte homeostasis,protect chondrocytes from oxidative stress,and promote the expression of autophagy related genes and the secretion of proteoglycan 4 by chondrocytes.(4)This paper details the molecular mechanism of FoxO1 regulation in different bone cells in detail,and elaborates the key role of FoxO1 in the treatment of bone-related diseases more comprehensive and deeply,providing new ideas for the treatment of osteoarthritis,osteoporosis,delayed fracture healing and other bone-related diseases.

Objective To assess the impact of freeze-drying and dry heat virus inactivation processes on the activity ofα2-macroglobulin(A2M)derived from human plasma Cohn fraction Ⅳ.Methods A2M derived from human plasma Cohn fraction Ⅳ was prepared and subjected to programmed freeze-drying with dry heat virus inactivation.The lyophilized products were evaluated for their appearance,water content,and validation of the viral inactivation process.The bioactivity of the products before and after lyophilization as well as before and after dry heat inactivation was determined via trypsin inhibition,and the comparisons were studied.Results The appearance of the lyophilized product was fluffy,and the water content was(5.83±0.45)％.The specific activities of the samples before and after lyophilization were(10.199±0.137)and(10.033±0.201)μg/mg,respectively,with no statistically significantdifference between the two groups(P＞0.05).The viral inactivation of the samples was carried out by using dry heat inactivation conditions at 100 ℃ for 30 min.After inactivation,the reduction was ≥5.125 LgTCID50/0.1 mL in Pseudorabies virus(PRV)titers,≥4.500 LgTCID50/0.1 mL in Sindbis virus(SinV)titers,≥6.375 LgTCID50/0.1 mL in encephalomyocarditis virus(EMCV)titers,and≥4.500 LgTCID50/0.1 mL in porcine parvovirus(PPV)titers.The specific activities of the samples before and after dry heat were(9.921±0.292)and(10.091±0.278)μ g/mg,respectively,with no statistically significant difference between the two groups.Conclusion A2M derived from human plasma Cohn fraction Ⅳ,when subjected to freeze-drying followed by dry heat inactivation at 100 ℃ for 30 minutes,can effectively inactivate viruses without altering the biological activity of the product.

Refinement and standardisation of the management of clinical diagnostic and treatment operations is a key aspect of achieving high-quality development in hospitals.By analysing the management status quo of clinical diagnosis and treatment operations in hospitals,it combed the problems existing in this field.Based on the closed-loop management model,it proposed measures and recommendations to promote the continuous optimisation of the management of clinical diagnostic operations in hospitals.Hospitals should establish hospital-level operation catalog and conduct classified management,authorize operators and dynamically adjust them,carry out operation quality management,pay attention to information management of operation management,and combine operation management with physician performance management.

Objective To explore the risk factors and incidence of epiretinal membrane(ERM)formation following scleral buckling(SB)for rhegmatogenous retinal detachment(RRD),and to construct a risk prediction model to facilitate screening of high-risk populations and prevent ERM formation.Methods RRD patients who underwent SB in the Second Affiliated Hospital of Harbin Medical University between February 2022 and April 2024 were included in the study.The pa-tients were divided into occurrence and non-occurrence groups according to whether they developed ERM.Patient data were analyzed,and univariate Cox regression analysis was performed to select variables,which were then incorporated into the multivariate Cox regression model for the identification of risk factors for ERM formation after SB in RRD patients.A predictive model for ERM risk in RRD patients was constructed based on this data,and nomograms,receiver operating characteristic(ROC)curves,and calibration curves were drawn to evaluate and validate the diagnostic performance of the model.Results A total of 126 RRD patients(126 eyes)who underwent SB were included.There were 27 cases develo-ping ERM(occurrence group)and 99 not developing ERM(non-occurrence group),with an ERM incidence of 21.4％.Multivariate Cox regression analysis revealed that a history of diabetes mellitus[Hazard ratio(HR)=3.52,95％CI:1.37-9.02,P=0.009],preoperative proliferative vitreoretinopathy(PVR)(HR=13.00,95％CI:5.18-32.63,P＜0.001),and ≥4 retinal holes(HR=2.33,95％CI:1.04-5.23,P=0.041)were independent influence factors for ERM formation in RRD patients.ROC curve analysis showed that the area under the curve(AUC)was 0.840(95％CI:0.740-0.940)at 30 days and 0.904(95％CI:0.834-0.975)at 90 days.Conclusion A history of diabetes mellitus,preoperative PVR,and ≥4 retinal holes are factors influencing the development of ERM after SB in RRD patients.It is verified that the risk prediction model constructed based on these factors can accurately predict the risk of ERM formation within 6 months in RRD patients.

Objective To elucidate the anti-aging effect of β-sitosterol(BS),an important component in the fruits of Alpinia oxyphylla Miq.,in C.elegans and its regulatory effect on ETS-5 gene to modulate ferroptosis.Methods C.elegans treated with 10 μg/mL BS were monitored for survival time and changes in body length,motility,and reproductive function.The effect of ETS-5 gene knockdown on survival time of C.elegans was observed,and the changes in fat accumulation and lipid redox homeostasis in the transfected C.elegans were assessed using Oil Red O staining and by detecting MDA levels and the GSH/GSSG ratio.The mRNA expression levels of ferroptosis-related genes(FTN-1,GPX-1 and AAT-9)were detected using qPCR.The effects of BS treatment and ETS-5 knockdown on AAT-9 enzyme activity in C.elegans were examined.The effect of BS on nuclear localization of FEV(the human homolog of ETS-5)was validated in cultured human umbilical venous endothelial cells(HUVECs).Results Both BS treatment and ETS-5 knockdown significantly prolonged the lifespan,promoted lipid accumulation and reduced lipid peroxidation in C.elegans.ETS-5 knockdown resulted in upregulated expressions of the ferroptosis repressors GPX-1,AAT-9 and FTN-1 and increased the GSH/GSSG ratio in C.elegans.Conclusion BS inhibits ferroptosis in C.elegans by suppressing the expression of ETS-5 transcription factor and hence the activity of AAT-9 enzyme,a key gene for ferroptosis,which in turn prolongs the lifespan of C.elegans.

ObjectiveTo evaluate pharmacological effects of Shengmai injection（SMI）on cerebral ischemia and study its neuroprotective mechanism. MethodsMale specific pathogen-free （SPF） Sprague-Dawley （SD） rats were randomly divided into a sham group， a model group， a low-dose SMI group（3 mL·kg^-1）， a middle-dose SMI group（6 mL·kg^-1）， a high-dose SMI group（12 mL·kg^-1）， and a Ginaton group（4 mL·kg^-1）according to the random number table method， with 12 rats in each group. The rat model of cerebral ischemia-reperfusion（MCAO/R）was prepared via the suture method. The administration groups were intraperitoneally injected with corresponding concentrations of SMI or Ginaton injection after reperfusion， which was conducted for 3 consecutive days. The sham group and model group were administered the equivalent volume of physiological saline. The pharmacological effects of SMI on brain injury in MCAO/R rats were evaluated by neurological function scores， cerebral infarction area， hematoxylin-eosin （HE） staining， Nissl staining， terminal deoxynucleotidyl transferase dUTP nick-end labeling （TUNEL） staining， and Western blot. The dominant link and key protein of SMI treating cerebral injury were explored using proteomic analysis. The related mechanisms of SMI were further validated using enzyme-linked immunosorbent assay （ELISA）， Western blot， and chloride ion fluorescence probe with oxygen-glucose deprivation/reoxygenation（OGD/R）-treated PC12 cells and MCAO/R rats. ResultsCompared with the sham group， the model group showed significantly increased neurological function scores， cerebral infarction area， neuronal apoptosis rate， and expression levels of apoptosis related proteins （P<0.05， P<0.01）and significantly decreased density of Nissl bodies and neurons（P<0.01）. Compared with the model group， the SMI groups exhibited significantly decreased neurological function scores， cerebral infarction area， neuronal apoptosis rate， and expression levels of apoptosis related proteins （P<0.05， P<0.01）and significantly increased density of Nissl bodies and neurons （P<0.05）. The proteomic analysis results showed that oxidative stress and inflammatory response were important processes of SMI intervening in MCAO/R injury， and the chloride intracellular channel protein 1 （CLIC1） was one of key proteins in its action network. The levels of representative indicators of oxidative stress and inflammatory response in the MCAO/R rats of the SMI groups were significantly reduced， compared with those in the model group（P<0.05， P<0.01）， and the expression levels of CLIC1 and downstream NOD-like receptor protein 3 （NLRP3） decreased （P<0.01）. In addition， the experimental results based on the OGD/R PC12 cells showed that SMI significantly increased the cell survival rate（P<0.01） and significantly decreased the intracellular chloride ion concentration（P<0.05）. ConclusionSMI has neuroprotective effects. Oxidative stress and inflammatory response are key processes of SMI intervening in MCAO/R injury. The potential mechanism is closely related to the regulation of CLIC1.

OBJECTIVES: To elucidate the anti-aging effect of β-sitosterol (BS), an important component in the fruits of Alpinia oxyphylla Miq., in C. elegans and its regulatory effect on ETS-5 gene to modulate ferroptosis. METHODS: C. elegans treated with 10 µg/mL BS were monitored for survival time and changes in body length, motility, and reproductive function. The effect of ETS-5 gene knockdown on survival time of C. elegans was observed, and the changes in fat accumulation and lipid redox homeostasis in the transfected C. elegans were assessed using Oil Red O staining and by detecting MDA levels and the GSH/GSSG ratio. The mRNA expression levels of ferroptosis-related genes (FTN-1, GPX-1 and AAT-9) were detected using qPCR. The effects of BS treatment and ETS-5 knockdown on AAT-9 enzyme activity in C. elegans were examined. The effect of BS on nuclear localization of FEV (the human homolog of ETS-5) was validated in cultured human umbilical venous endothelial cells (HUVECs). RESULTS: Both BS treatment and ETS-5 knockdown significantly prolonged the lifespan, promoted lipid accumulation and reduced lipid peroxidation in C. elegans. ETS-5 knockdown resulted in upregulated expressions of the ferroptosis repressors GPX-1, AAT-9 and FTN-1 and increased the GSH/GSSG ratio in C. elegans. CONCLUSIONS BS inhibits ferroptosis in C. elegans by suppressing the expression of ETS-5 transcription factor and hence the activity of AAT-9 enzyme, a key gene for ferroptosis, which in turn prolongs the lifespan of C. elegans.
Animals ; Caenorhabditis elegans/physiology* ; Ferroptosis/drug effects* ; Alpinia/chemistry* ; Sitosterols/pharmacology* ; Longevity/drug effects* ; Fruit/chemistry* ; Humans