ObjectiveThis paper aims to explore the in vitro anti-psoriasis activity and potential mechanism of Kangfuxin liquid （KFX liquid）， providing experimental evidence for the anti-psoriasis effect of KFX liquid. MethodsFirstly， the uninduced human immortalized keratinocyte cells （HaCaT cells） were divided into seven groups， namely the control group and KFX liquid groups with different doses （5， 10， 20， 40， 80， 160 g·L^-1）. After being treated with different concentrations of KFX liquid， the effect of KFX liquid on the normal cell proliferation was detected by using the cell counting kit-8 （CCK-8） method. Secondly， the uninduced HaCaT cells were divided into six groups， namely the control group and recombinant human interleukin-7A （rh-IL-7A） groups with different doses （5， 10， 50， 100， 120 g·L^-1）. After being treated with different concentrations of recombinant human interleukin-17A （rh IL-17A） liquid， the effect of rh IL-17A on cell proliferation was detected. The optimal induction concentration was screened. Then， normal HaCaT cells were divided into a control group and KFX liquid groups with different doses （5， 10， 20， 40， 80， 160 g·L^-1）. Except for the control group， the other groups established psoriasis cell models with the optimal induction concentration of rh IL-17A. After being treated with different concentrations of KFX liquid， the effects of KFX liquid on the psoriasis-like HaCaT cell proliferation were investigated. Finally， the uninduced HaCaT cells were divided into six groups， namely the control group， rh IL-17A group， methotrexate （MTX） group， and KFX liquid groups with different doses （20， 40， 80 g·L^-1）. Except for the control group， the other groups used the optimal induction concentration of rh IL-17A to establish psoriasis cell models. After being treated with different drugs， the cell migration levels were detected through scratch assays， and real-time quantitative polymerase chain reaction （Real-time PCR） was used to detect the relative mRNA expression levels of Ki-67 antigen （Ki67）， S100 calcium-binding protein A7 （S100A7）， S100 calcium-binding protein A8 （S100A8）， and S100 calcium-binding protein A9 （S100A9）， thereby comprehensively evaluating the in vitro anti-psoriasis activity of KFX liquid. By detecting the relative mRNA expression levels of interleukin-1β （IL-1β）， interleukin-6 （IL-6）， and chemokine-20 （CXCL-20） inflammatory-related factors in psoriasis-like HaCaT cells and the protein expression levels of Janus kinase 3 （JAK3）， phosphorylated Janus kinase 3 （p-JAK3）， signal transducer and activator of transcription 3 （STAT3）， and phosphorylated signal transducer and activator of transcription 3 （p-STAT3）， the mechanism was explored. ResultsCompared with that of control group， when treated with 80 g·L^-1 KFX liquid for 72 h （P<0.05） and at different times with 160 g·L^-1 KFX liquid， the HaCaT cell proliferation activity was significantly affected （P<0.01）， while the other concentrations of KFX liquid had no significant differences in cell morphology and cell proliferation activity at different times， indicating that the KFX liquid is relatively safe for HaCaT cells and has no obvious toxic side effects. Compared with that of control group， when treated with different concentrations of rh IL-17A for 24 h， the HaCaT cell proliferation activity was significantly enhanced， and the cell activity was the strongest when the concentration was 100 μg·L^-1 （P<0.05）， with a density close to 100% and intact cell morphology， indicating that 100 μg·L^-1 is the optimal concentration for inducing HaCaT cell proliferation. The results of the KFX liquid treatment on rh IL-17A-induced psoriasis-like cells show that the KFX liquid not only effectively inhibits the rh IL-17A-induced psoriasis-like HaCaT cell proliferation activity （P<0.01）， but also significantly reduces the migration ability of rh IL-17A-induced psoriasis-like HaCaT cells （P<0.01）， and the relative mRNA expression levels of Ki67， S100A7， S100A8， and S100A9 （P<0.01）. Moreover， the KFX liquid can significantly reduce the relative mRNA expression levels of IL-1β， IL-6， and CXCL-20 in rh IL-17A-induced psoriasis-like cells （P<0.01）， and significantly inhibit the phosphorylation levels of JAK3 and STAT3 proteins （P<0.05， P<0.01）. ConclusionThe KFX liquid has no obvious toxicity to uninduced HaCaT cells. It can inhibit rh IL-17A-induced psoriasis-like HaCaT cell proliferation， reduce the cell migration ability， and has good in vitro anti-psoriasis activity. Its action mechanism may be related to downregulating the expression levels of inflammation-related cytokines in the JAK3/STAT3 signaling pathway and inhibiting the phosphorylation levels of JAK3 and STAT3 proteins.

ObjectiveThis paper aims to explore the in vitro anti-psoriasis activity and potential mechanism of Kangfuxin liquid （KFX liquid）， providing experimental evidence for the anti-psoriasis effect of KFX liquid. MethodsFirstly， the uninduced human immortalized keratinocyte cells （HaCaT cells） were divided into seven groups， namely the control group and KFX liquid groups with different doses （5， 10， 20， 40， 80， 160 g·L^-1）. After being treated with different concentrations of KFX liquid， the effect of KFX liquid on the normal cell proliferation was detected by using the cell counting kit-8 （CCK-8） method. Secondly， the uninduced HaCaT cells were divided into six groups， namely the control group and recombinant human interleukin-7A （rh-IL-7A） groups with different doses （5， 10， 50， 100， 120 g·L^-1）. After being treated with different concentrations of recombinant human interleukin-17A （rh IL-17A） liquid， the effect of rh IL-17A on cell proliferation was detected. The optimal induction concentration was screened. Then， normal HaCaT cells were divided into a control group and KFX liquid groups with different doses （5， 10， 20， 40， 80， 160 g·L^-1）. Except for the control group， the other groups established psoriasis cell models with the optimal induction concentration of rh IL-17A. After being treated with different concentrations of KFX liquid， the effects of KFX liquid on the psoriasis-like HaCaT cell proliferation were investigated. Finally， the uninduced HaCaT cells were divided into six groups， namely the control group， rh IL-17A group， methotrexate （MTX） group， and KFX liquid groups with different doses （20， 40， 80 g·L^-1）. Except for the control group， the other groups used the optimal induction concentration of rh IL-17A to establish psoriasis cell models. After being treated with different drugs， the cell migration levels were detected through scratch assays， and real-time quantitative polymerase chain reaction （Real-time PCR） was used to detect the relative mRNA expression levels of Ki-67 antigen （Ki67）， S100 calcium-binding protein A7 （S100A7）， S100 calcium-binding protein A8 （S100A8）， and S100 calcium-binding protein A9 （S100A9）， thereby comprehensively evaluating the in vitro anti-psoriasis activity of KFX liquid. By detecting the relative mRNA expression levels of interleukin-1β （IL-1β）， interleukin-6 （IL-6）， and chemokine-20 （CXCL-20） inflammatory-related factors in psoriasis-like HaCaT cells and the protein expression levels of Janus kinase 3 （JAK3）， phosphorylated Janus kinase 3 （p-JAK3）， signal transducer and activator of transcription 3 （STAT3）， and phosphorylated signal transducer and activator of transcription 3 （p-STAT3）， the mechanism was explored. ResultsCompared with that of control group， when treated with 80 g·L^-1 KFX liquid for 72 h （P<0.05） and at different times with 160 g·L^-1 KFX liquid， the HaCaT cell proliferation activity was significantly affected （P<0.01）， while the other concentrations of KFX liquid had no significant differences in cell morphology and cell proliferation activity at different times， indicating that the KFX liquid is relatively safe for HaCaT cells and has no obvious toxic side effects. Compared with that of control group， when treated with different concentrations of rh IL-17A for 24 h， the HaCaT cell proliferation activity was significantly enhanced， and the cell activity was the strongest when the concentration was 100 μg·L^-1 （P<0.05）， with a density close to 100% and intact cell morphology， indicating that 100 μg·L^-1 is the optimal concentration for inducing HaCaT cell proliferation. The results of the KFX liquid treatment on rh IL-17A-induced psoriasis-like cells show that the KFX liquid not only effectively inhibits the rh IL-17A-induced psoriasis-like HaCaT cell proliferation activity （P<0.01）， but also significantly reduces the migration ability of rh IL-17A-induced psoriasis-like HaCaT cells （P<0.01）， and the relative mRNA expression levels of Ki67， S100A7， S100A8， and S100A9 （P<0.01）. Moreover， the KFX liquid can significantly reduce the relative mRNA expression levels of IL-1β， IL-6， and CXCL-20 in rh IL-17A-induced psoriasis-like cells （P<0.01）， and significantly inhibit the phosphorylation levels of JAK3 and STAT3 proteins （P<0.05， P<0.01）. ConclusionThe KFX liquid has no obvious toxicity to uninduced HaCaT cells. It can inhibit rh IL-17A-induced psoriasis-like HaCaT cell proliferation， reduce the cell migration ability， and has good in vitro anti-psoriasis activity. Its action mechanism may be related to downregulating the expression levels of inflammation-related cytokines in the JAK3/STAT3 signaling pathway and inhibiting the phosphorylation levels of JAK3 and STAT3 proteins.

Objective To investigate the antibacterial activity of the antifungal peptide Mt6-21DLeu derived from Musca domestica against Acinetobacter baumannii (AB) and unravel its underlying mechanisms, so as to provide insights into development of novel agents against AB. Methods The minimum inhibitory concentrations (MICs) of Mt6-21DLeu, M. domestica-derived antifungal peptide-1 (MAF-1A), and polymyxin B were determined against Staphylococcus aureus, Bacillus subtilis, Escherichia coli, Klebsiella pneumoniae, Pseudomonas aeruginosa and AB using the broth microdilution assay, and the antibacterial activity of Mt6-21DLeu and polymyxin B was dynamically assessed against AB over 24 hours with time-kill curves. The inhibitory effects of Mt6-21DLeu and polymyxin B on biofilm formation in AB at concentrations of 1/4 × MIC, 1/2 × MIC and MIC, and the eradication effects of Mt6-21DLeu and polymyxin B on mature biofilms in AB at concentrations of MIC, 2 × MIC, and 4 × MIC were evaluated using crystal violet staining. Structural changes in the cell membrane of AB were observed 3 hours post-exposure to Mt6-21DLeu at concentrations of MIC and 2 × MIC using scanning electron microscopy, and alterations in the cell membrane permeability of AB were analyzed 3 hours post-treatment with Mt6-21DLeu at concentrations of MIC and 2 × MIC by means of fluorescence microscopy and propidium iodide (PI) staining. Intracellular reactive oxygen species (ROS) levels in AB were measured 3 hours post-treatment with Mt6-21DLeu at concentrations of MIC, 2 × MIC, and 4 × MIC using flow cytometry. The survival of Caenorhabditis elegans exposed to Mt6-21DLeu at concentrations of MIC, 2 × MIC, and 4 × MIC was monitored for 7 consecutive days, and survival curves were plotted to evaluate the in vivo toxicity of Mt6-21DLeu. In addition, C. elegans infected with AB and treated with Mt6-21DLeu at a concentration of 4 × MIC served as the treatment group, and uninfected C. elegans served as the control group, while infected but untreated C. elegans served as the infection group. The in vivo antibacterial efficacy of Mt6-21DLeu at a concentration of 4 × MIC was evaluated by comparing the survival curves and bacterial load among the three groups. Results The MICs of MAF-1A were all >128 μg/mL against S. aureus, B. subtilis, E. coli, K. pneumoniae, P. aeruginosa, and AB. In contrast, the MICs of Mt6-21DLeu were >128, 32, 8, 8, 16, and 4 μg/mL against these strains, respectively, and the MIC of Mt6-21DLeu against AB was close to that of polymyxin B (2 μg/mL). Time-kill curve analysis showed that both Mt6-21DLeu at concentrations of MIC and 2 × MIC and polymyxin B at a concentration of MIC inhibited AB growth over the 24-hour study period. The biofilm biomass in AB was (52.38 ± 6.92)%, (40.88 ± 9.17)% and (14.77 ± 6.00)% post-exposure with Mt6-21DLeu at concentrations of 1/4 × MIC, 1/2 × MIC and MIC, (61.58 ± 7.35)%, (47.42 ± 5.51)% and (20.85 ± 10.48)% post-treatment with polymyxin B at concentrations of 1/4 × MIC, 1/2 × MIC and MIC, and (100.00 ± 15.92)% in the control group (only bacterial suspension), respectively (F = 68.38, P < 0.001), and pairwise comparisons indicated that Mt6-21DLeu and polymyxin B at all concentrations significantly inhibited biofilm formation as compared to the control group (all P values < 0.001). The mature biofilm biomass in AB was (73.44 ± 11.41)%, (72.56 ± 13.08)% and (49.65 ± 9.23)% post-exposure to Mt6-21DLeu at concentrations of MIC, 2 × MIC, and 4 × MIC, (84.38 ± 8.60)%, (72.31 ± 9.63)% and (58.85 ± 4.96)% post-treatment with polymyxin B at concentrations of MIC, 2 × MIC, and 4 × MIC, and (100.00 ± 6.36)% in the control group (F = 35.63, P < 0.001), and pairwise comparisons revealed that Mt6-21DLeu at all concentrations significantly eradicated biofilm biomass (all P values < 0.05); however, polymyxin B showed no clear-cut eradication effect at a concentration of MIC (P > 0.05). Scanning electron microscopy revealed pore formation and content leakage in the cell membrane of AB 3 hours post-treatment with Mt6-21DLeu at concentrations of MIC and 2 × MIC. Fluorescence microscopy showed that the proportions of PI-stained AB were (24.79 ± 11.51)% and (68.44 ± 15.80)% post-treatment with Mt6-21DLeu at concentrations of MIC and 2 × MIC, and (0.96 ± 0.94)% in the phosphate-buffered saline (PBS) treatment group (F = 105.90, P < 0.001), with the highest proportion of PI-stained AB seen post-treatment with Mt6-21DLeu at a concentration of 2 × MIC (P < 0.05). Flow cytometry revealed that the relative intracellular ROS levels in AB were (652.00 ± 141.90), (694.33 ± 14.19), and (974.33 ± 160.02) 3 hours post-treatment with Mt6-21DLeu at concentrations of MIC, 2 × MIC and 4 × MIC, and (403.67 ± 86.56) in the PBS treatment group, respectively (F = 12.27, P < 0.05), with the highest intracellular ROS level measured following treatment with Mt6-21DLeu at a concentration of 4 × MIC (P < 0.05). Survival curve analysis revealed that Mt6-21DLeu posed no impact on C. elegans survival at concentrations of MIC (χ² = 0.02, P > 0.05), 2 × MIC (χ² = 0.06, P > 0.05) or 4 × MIC (χ² = 0.16, P > 0.05), and there was a significant difference in the survival period of C. elegans among the control group, the infection group, and the treatment group (χ² = 82.66, P < 0.05), with a significantly longer survival period in the treatment group than in the infection group (χ² = 45.00, P < 0.05). In addition, the log-transformed bacterial colony counts in C. elegans were (0.00 ± 0.00), (5.46 ± 0.03), and (3.91 ± 0.47) CFU/mL in the control group, the infection group, and the treatment group, respectively (F = 324.80, P < 0.001), and the log-transformed bacterial colony counts in C. elegans were significantly lower in the treatment group than in the infection group (P < 0.05). Conclusions Mt6-21DLeu exerts potent antibacterial effects through disrupting the cell membrane integrity of AB and promoting intracellular ROS accumulation in AB, and exhibits promising potential for treatment of AB infections both in vivo and in vitro, which may serve as a candidate drug molecule against multidrug-resistant AB infections.

Jiuwei Xifeng Granules have become a Chinese patent medicine in the market. Because the formula contains Os Draconis, a top-level protected fossil of ancient organisms, the formula was to be improved by replacing Os Draconis with Ostreae Concha. To evaluate whether the improved formula has the same effectiveness and safety as the original formula, a randomized, double-blind, parallel-controlled, equivalence clinical trial was conducted. This study enrolled 288 tic disorder(TD) of children and assigned them into two groups in 1∶1. The treatment group and control group took the modified formula and original formula, respectively. The treatment lasted for 6 weeks, and follow-up visits were conducted at weeks 2, 4, and 6. The primary efficacy endpoint was the difference in Yale global tic severity scale(YGTSS)-total tic severity(TTS) score from baseline after 6 weeks of treatment. The results showed that after 6 weeks of treatment, the declines in YGTSS-TSS score showed no statistically significant difference between the two groups. The difference in YGTSS-TSS score(treatment group-control group) and the 95%CI of the full analysis set(FAS) were-0.17[-1.42, 1.08] and those of per-protocol set(PPS) were 0.29[-0.97, 1.56], which were within the equivalence boundary [-3, 3]. The equivalence test was therefore concluded. The two groups showed no significant differences in the secondary efficacy endpoints of effective rate for TD, total score and factor scores of YGTSS, clinical global impressions-severity(CGI-S) score, traditional Chinese medicine(TCM) response rate, or symptom disappearance rate, and thus a complete evidence chain with the primary outcome was formed. A total of 6 adverse reactions were reported, including 4(2.82%) cases in the treatment group and 2(1.41%) cases in the control group, which showed no statistically significant difference between the two groups. No serious suspected unexpected adverse reactions were reported, and no laboratory test results indicated serious clinically significant abnormalities. The results support the replacement of Os Draconis by Ostreae Concha in the original formula, and the efficacy and safety of the modified formula are consistent with those of the original formula.
Adolescent ; Child ; Child, Preschool ; Female ; Humans ; Male ; Double-Blind Method ; Drugs, Chinese Herbal/therapeutic use* ; Tic Disorders/drug therapy* ; Treatment Outcome

The real-time Delphi method represents a refinement of the classical Delphi technique, designed to overcome limitations such as prolonged study duration and delayed feedback during consensus development. This article, building upon the classical Delphi foundation, systematically elaborates on the application process, advantages, and limitations of the real-time Delphi method. It further presents currently available websites or software capable of facilitating real-time Delphi exercises and offers considerations and recommendations for its application in guideline development, aiming to serve as a reference for relevant researchers.

Objective:To investigate the protective effect of lovastatin on liver injury in the rats induced by hyperlipidemia,and to elucidate its possible mechanism.Methods:Fifteen SD rats were randomly divided into control group,hyperlipidemia model group,and lovastatin group,with 5 rats in each group.The rats in control group were fed with standard diet,while the rats in hyperlipidemia model group and lovastatin group were fed high-fat diet for 12 weeks.Starting from the 8th week,the rats were administered treatments via gavage once a day for 4 weeks:the rats in lovastatin group received 2 mng·kg-1 lovastatin,while the rats in control group and hyperlipidemia model group received an equal volume of normal saline.The body weights of the rats in various groups were measured at weeks 1,8,9,10,11,and 12 after the experiment began;the histopathology of liver tissue of the rats in various groups was observed using HE staining;the serum levels of total cholesterol(TC),triglycerides(TG),high-density lipoprotein cholesterol(HDL-C),low-density lipoprotein cholesterol(LDL-C),malondialdehyde(MDA),as well as the activities of superoxide dismutase(SOD),glutathione peroxidase(GSH-Px),aspartate aminotransferase(AST),and alanine aminotransferase(ALT),and the levels of interleukin-2(IL-2),interleukin-6(IL-6),interleukin-12(IL-12),and tumor necrosis factor-a(TNF-α)of the rats in various groups were detected using commercial kits;the composition of the gut microbiota of the rats in various groups was analyzed by 16S rRNA sequencing.Results:Compared with control group,the body weight of the rats in hyperlipidemia model group was significantly increased from the 8th week of high-fat diet feeding(P＜0.05 or P＜0.01 or P＜0.001).Compared with hyperlipidemia model group,the body weight of the rats in lovastatin group was significantly decreased at weeks 11 and 12(P＜0.05).Compared with control group,the livers of the rats in hyperlipidemia model group appeared rough,pale,enlarged,with blunt edges,and had a granular and greasy texture.Compared with hyperlipidemia model group,the livers of the rats in lovastatin group were light brownish-red,soft,with slightly blunt edges,reduced volume,and less granularity and greasiness.Compared with control group,the liver cells of the rats in hyperlipidemia model group were swollen and disorganized,with pyknotic nuclei,extensive inflammatory cell infiltration,and numerous vacuolar degenerations.Compared with hyperlipidemia model group,the rats in lovastatin group showed significantly reduced hepatocyte swelling and degeneration,more orderly and intact liver cell arrangement,decreased inflammatory cell infiltration,and reduced vacuolar degeneration.Compared with control group,the serum levels of TC,TG,and LDL-C of the rats in hyperlipidemia model group were significantly increased(P＜0.05),and the serum HDL-C level was decreased(P＜0.05).Compared with hyperlipidemia model group,the serum levels of TC,TG,and LDL-C of the rats in lovastation group were significantly decreased(P＜0.05),and the serum HDL-C level was increased(P＜0.05).Compared with control group,the serum MDA levels and the ALT and AST activities of the rats in hyperlipidemia model group were significantly increased(P＜0.05),and the SOD and GSH-Px activities were significantly decreased(P＜0.05).Compared with hyperlipidemia model group,the serum MDA levels and ALT and AST activities of the rats in lovastatin group were decreased(P＜0.05),and the SOD and GSH-Px activities were increased(P＜0.05).Compared with control group,the serum levels of IL-2,IL-6,IL-12,and TNF-α of the rats in hyperlipidemia model group were significantly increased(P＜0.05).Compared with hyperlipidemia model group,the serum levels of IL-2,IL-6,IL-12,and TNF-α of the rats in lovastatin group were significantly decreased(P＜0.05).Compared with control group,the ACE and Chao1 indexes of the rats in hyperlipidemia model group were significantly decreased(P＜0.05).Compared with hyperlipidemia model group,the ACE and Chao1 indexes of the rats in lovastatin group were significantly increased(P＜0.05 or P＜0.01).Compared with control group,the relative abundances of Firmicutes and Proteobacteria of the rats in hyperlipidemia model group were significantly increased(P＜0.001),and the relative abundances of Bacteroidetes and Actinobacteria were decreased(P＜0.001).Compared with hyperlipidemia model group,the relative abundances of Firmicutes and Proteobacteria of the rats in lovastatin group were significantly decreased(P＜0.05 or P＜0.01),while the relative abundances of Bacteroidetes and Actinobacteria showed no significant changes.Compared with control group,the relative abundance of Lactobacillus of the rats in hyperlipidemia model group was significantly decreased(P＜0.001),and the relative abundances of Bacteroides,Desulfovibrio,and Clostridium were significantly increased(P＜0.01 or P＜0.001).Compared with hyperlipidemia model group,the relative abundance of Lactobacillus of the rats in lovastatin group showed no significant change but the relative abundances of Bacteroides,Desulfovibrio,and Clostridium were significantly decreased(P＜0.05 or P＜0.01 or P＜0.001).Conclusion:Lovastatin ameliorates liver injury induced by hyperlipidemia,and the mechanism may be related to its ability to improve gut microbiota composition and inhibit oxidative stress and inflammatory damage.

Objective To study the inhibitory effect of secondary metabolites of Pseudomonas aeruginosa(PA)on Candida albicans(CA)and to explore some of the mechanisms.Methods PA and CA strains were i-solated from clinical specimens from the hospital.Then,PA strains with inhibitory effects on CA were screened through cross-line test and co-incubation test,and crude extracts of PA secondary metabolites were prepared,and were tested together with pyocyanin,phenazine-1-carboxylic acid,1-hydroxyphenazine,and 3-ox-ododecyl-l-homoserine lactone(3-oxo-HSL).The inhibitory effects of various PA secondary metabolites on CA were determined through minimum inhibitory concentration test,minimum bactericidal concentration test,time-sterilization curve measurement,and XTT method activity measurement test,and some mechanisms by which PA secondary metabolites inhibited CA were explored.Results The strongest inhibitory effect on CA was 1-hydroxyphenazine,and at a concentration of 6.250 μg/mL,the relative activity of CA decreased to 0.00%.Next were pyocyanin and PA crude extract,and the relative fungal activity of CA decreased to 0.00%at concentrations of 200 and 100 μg/mL.1-hydroxyphenazine,pyocyanin,3-oxo-HSL and PA crude extract all had inhibitory effects on the formation of CA hyphae.Reactive oxygen species(ROS)were generated in CA cells treated with 1-hydroxyphenazine,phenazine 1-carboxylic acid,pyocyanin,and PA crude extract,and the highest levels of ROS were induced by pyocyanin and 1-hydroxyphenazine.Conclusion Phenazine secondary metabolites 1-hydroxyphenazine and pyocyanin have significant inhibitory effects on the growth and activity of CA,and both induce the highest amount of ROS.The quorum-sensing signal molecule 3-oxo-HSL have no in-hibitory effect on CA growth,but have a significant inhibitory effect on the formation of fungal hyphae.

OBJECTIVE To investigate the incidence of hospital-associated infections among the neurosurgery de-partment patients undergoing brain tumor resection and analyze the economic cost so as to provide scientific bases for formulating prevention strategies.METHODS Totally 1027 patients who underwent brain tumor resection in neurosurgery department of the First Affiliated Hospital of Shandong First Medical University from Jan.1,2020 to Dec.31,2024 were recruited as the research subjects.The 36 patients who had postoperative hos-pital-associated infections were assigned as the infection group,and 991 patients who did not have hospital-associ-ated infection were assigned as the no infection group.The patients of the infection group and the non-infection group were matched in a 1∶1 ratio by using propensity score matching method(caliper value 0.005).The length of hospital stay and costs of medical items were compared between the infection group and the non-infection group,and the economic burden due to the hospital-associated infections was estimated.RESULTS The incidence of hospital-associated infections was 3.51％among the patients undergoing brain tumor resection,and totally 36 pairs were matched successfully with the propensity score.The hospitalization cost of the infection group was 109,103.81(73,370.21,163,628.37)yuan after the matching,which was increased by 50,087.69 yuan as com-pared with the non-infection group(Z=-5.237,P＜0.001);the length of hospital stay was 23.00(17.25,36.00)days,which was prolonged by 8.50 days(Z=-3.764,P＜0.001).Among the costs of medical items,the medial costs of western medicine,treatment materials and clinical laboratory tests increased most.CONCLUSIONS The control of the costs of western medicine,treatment materials and clinical laboratory tests is the key to reduce the costs of brain tumor resection patients with hospital-associated infections.It is necessary to carry out the real-time monitoring of the hospital-associated infections and early warning of suspected cases and reduce the incidence of hospital-associated infections so as to reduce the economic costs.

In recent years, with the rapid development of artificial intelligence technology, the application of deep learning in the field of pathology has been continuously expanding. Particularly, the rise of multimodal data fusion methods has opened up new technical paths for the precise diagnosis, prognosis assessment, and individualized treatment of tumors. By integrating multi-level and multi-source data such as clinical information, pathological omics, molecular omics, and imaging omics, deep learning models can identify potential associated features and key biological mechanisms that are difficult to reveal by a single modality, thereby significantly improving the accuracy of disease classification and the scientific nature of risk stratification. This article systematically reviews the research progress of multimodal data fusion methods based on deep learning in the field of pathology in recent years, focuses on sorting out different types of fusion strategies, evaluates their advantages and challenges in practical clinical applications, and looks forward to future development trends.

Objective To investigate the structural changes and influencing factors of the average inpatient cost per admis-sion in public hospitals in Guangdong Province.Methods Grey relational analysis and structural variation degree analysis were used to analyze the correlation and changes between the average inpatient cost per admission and various cost components in public hospitals of Guangdong Province from 2017 to 2023.Results The average inpatient cost per admission in public hospitals of Guangdong Province showed an overall upward trend from 2017 to 2023,with an average annual growth rate of 3.84％.Among the components,laboratory test fees and examination fees grew at average annual rates of 6.17％and 6.68％,respectively.The top four cost components with the highest grey relational degree with the average inpatient cost were laboratory test fees(0.867),exam-ination fees(0.835),nursing fees(0.784),and treatment fees(0.728).The top four components with the largest structural vari-ation values were surgery fees(2.57％),medical material fees(1.77％),laboratory test fees(1.56％),and examination fees(1.45％).Conclusion The growth of the average inpatient cost per admission has slowed,and the cost structure has been opti-mized to some extent.However,the relatively rapid increase in laboratory test and examination fees has a significant impact on the cost structure.It is necessary to deepen the coordinated governance of healthcare,medical insurance,and medicine,strengthen the leveraging role of medical insurance payment,improve the external governance system and scientific compensation mechanism,and combine these with refined hospital management to promote reasonable cost control and high-quality development in public hospitals.