BACKGROUND:During diabetic wound healing,the sustained activation of M1 macrophages exacerbates the inflammatory response and hinders wound repair.Auranofin,an anti-inflammatory drug,has not been clearly studied for its effects on M1 macrophages and its potential role in diabetic wound healing.OBJECTIVE:To investigate the effects of different concentrations of auranofin on the biological function of M1 macrophages and evaluate its potential application in diabetic wound healing.METHODS:RAW264.7 and THP-1 cells were used as research models.M1 polarization was induced using different concentrations of interferon-γ and lipopolysaccharide.M1 macrophages were treated with 1 and 2 μmol/L auranofin.Cell counting kit-8 assay was used to evaluate the effect of auranofin on cell viability.Quantitative real-time PCR was performed to detect mRNA expression of interleukin-1β,interleukin-6,and tumor necrosis factor-α.ELISA was employed to measure the levels of interleukin-1β,interleukin-6,and tumor necrosis factor-α in the supernatant.Western blot analysis was used to assess the expression of nuclear factor-κB(p65),phosphorylated mitogen-activated protein kinases(MAPK),and total MAPK proteins.Additionally,6-8-week-old male C57BL/6J and db/db diabetic mice were used for wound healing experiments,with the mice divided into C57 control,db/db control and auranofin treatment groups,each containing six animals.Dorsal skin defect modeling and treatment with intraperitoneal injection of auranofin were performed to observe wound healing in mice.RESULTS AND CONCLUSION:(1)Cell experiments showed that co-treatment with interferon-y(10 ng/mL)and lipopolysaccharide(100 ng/mL)significantly induced M1 polarization in RAW264.7 and THP-1 cells,resulting in increased mRNA expression of interleukin-1β,interleukin-6,and tumor necrosis factor-α.Treatment with auranofin(1 and 2 μmol/L)reduced the mRNA expression of these inflammatory factors in the cells and inhibited the secretion of inflammatory factors in the cell supernatant.(2)Auranofin treatment significantly suppressed the activation of nuclear factor-κB(p65)and phosphorylated MAPK signaling pathways.(3)Animal experiments showed that auranofin promoted wound healing in db/db diabetic mice,suggesting that auranofin has strong anti-inflammatory effects and may facilitate the healing of wounds in diabetic mice.

BACKGROUND:During diabetic wound healing,the sustained activation of M1 macrophages exacerbates the inflammatory response and hinders wound repair.Auranofin,an anti-inflammatory drug,has not been clearly studied for its effects on M1 macrophages and its potential role in diabetic wound healing.OBJECTIVE:To investigate the effects of different concentrations of auranofin on the biological function of M1 macrophages and evaluate its potential application in diabetic wound healing.METHODS:RAW264.7 and THP-1 cells were used as research models.M1 polarization was induced using different concentrations of interferon-γ and lipopolysaccharide.M1 macrophages were treated with 1 and 2 μmol/L auranofin.Cell counting kit-8 assay was used to evaluate the effect of auranofin on cell viability.Quantitative real-time PCR was performed to detect mRNA expression of interleukin-1β,interleukin-6,and tumor necrosis factor-α.ELISA was employed to measure the levels of interleukin-1β,interleukin-6,and tumor necrosis factor-α in the supernatant.Western blot analysis was used to assess the expression of nuclear factor-κB(p65),phosphorylated mitogen-activated protein kinases(MAPK),and total MAPK proteins.Additionally,6-8-week-old male C57BL/6J and db/db diabetic mice were used for wound healing experiments,with the mice divided into C57 control,db/db control and auranofin treatment groups,each containing six animals.Dorsal skin defect modeling and treatment with intraperitoneal injection of auranofin were performed to observe wound healing in mice.RESULTS AND CONCLUSION:(1)Cell experiments showed that co-treatment with interferon-y(10 ng/mL)and lipopolysaccharide(100 ng/mL)significantly induced M1 polarization in RAW264.7 and THP-1 cells,resulting in increased mRNA expression of interleukin-1β,interleukin-6,and tumor necrosis factor-α.Treatment with auranofin(1 and 2 μmol/L)reduced the mRNA expression of these inflammatory factors in the cells and inhibited the secretion of inflammatory factors in the cell supernatant.(2)Auranofin treatment significantly suppressed the activation of nuclear factor-κB(p65)and phosphorylated MAPK signaling pathways.(3)Animal experiments showed that auranofin promoted wound healing in db/db diabetic mice,suggesting that auranofin has strong anti-inflammatory effects and may facilitate the healing of wounds in diabetic mice.

ObjectiveTo investigate the application of central auditory testing combined with electroencephalographic features in the early screening of mild cognitive impairment due to Alzheimer's disease. MethodsA convenience sampling method was used to conduct a field survey in the Qixia District of Nanjing City, Jiangsu Province, from July to September, 2025. A total of 40 older adults diagnosed as mild cognitive impairment due to Alzheimer's disease and 23 cognitively normal older adults were recruited. Auditory N-back and dichotic listening paradigms were employed for assessment, while the scores of Montreal Cognitive Assessment Beijing Version (MoCA-BJ) and 32-channel electroencephalogram (EEG) data were simultaneously collected. Binary logistic regression analysis was applied to identify predictive indicators, receiver operating characteristic (ROC) curves were plotted, and the area under the curve (AUC) was calculated. ResultsThe total score of dichotic listening was positively correlated with overall cognitive function (r = 0.475, P < 0.01), while right-ear advantage showed negative correlations with overall cognition, visuospatial ability, abstract reasoning, and delayed recall (r < -0.276, P < 0.05). Task performance across all conditions of the N-back task was positively correlated with overall cognitive function (r > 0.249, P < 0.05). Regarding EEG features, δ and θ band power and power peaks were positively correlated with delayed recall (r > 0.258, P < 0.05), whereas (α+θ)/(α+β) and θ/(α+β) were positively correlated with naming ability and visuospatial executive function, respectively (r > 0.261, P < 0.05). The results of the binary logistic regression analysis showed that the total score of binaural dichotic listening, the accuracy of 1-back task, the average power of δ waves, and the ratio of θ/(α+β) were independent influencing factors for mild cognitive impairment due to Alzheimer's disease (P < 0.05). The ROC analysis indicated that the AUC for auditory task performance and EEG features were 0.845 and 0.735 respectively, and when combined, the AUC increased to 0.862. ConclusionThe screening model based on the integration of auditory task performance and EEG features can be used in the early identification of mild cognitive impairment due to Alzheimer's disease.

Objective To investigate the effect of tritiated water on the immune system of zebrafish and its potential molecular mechanism. Methods Zebrafish embryos (2.5 to 3 hours post-fertilization [hpf]) were exposed to 3.7 × 10⁴ Bq/mL tritiated water (tritiated water group), and those exposed to E3 culture medium were used as the control group. The mortality rate, hatching rate, deformity rate, heart rate, body length, yolk sac area, neutrophil count in the tail, immune-related gene expression, and immune-related protein expression of zebrafish in the two groups were determined. Then transcriptome technology was used to further analyze the possible mechanism of tritiated water affecting the immune system of zebrafish. Results Compared with the control group, zebrafish at 72 hpf in the tritiated water group had no significant changes in the mortality rate, hatching rate, deformity rate, body length, and yolk sac area((t = 0.9045, 0.5000, 1.0000, 0.7238, 0.0337, P = 0.4169, 0.6433, 0.3739, 0.4785, 0.9735), but had significantly increased heart rate(t = 4.575，P = 0.002). At 4 days post-fertilization (dpf), the neutrophil count in the tail of zebrafish in the tritiated water group was significantly increased(t = 2.563，P = 0.0196), the mRNA expression of TNF-α was significantly decreased(t = 2.891, P = 0.045), the protein expression of nuclear factor-kappa B (NF-κB) was significantly increased(t = 3.848, P = 0.018), and the protein expression of NLRP3 was significantly decreased(t = 14.98, P = 0.001). At 7 dpf, the neutrophil count in the tail and the protein expression levels of NF-κB, NLRP3, and interleukin-1β were significantly decreased(t = 3.772, 7.048, 15.620, 4.423, P = 0.014, 0.002, 0.0001, 0.012). Transcriptome sequencing revealed that differentially expressed genes were mainly enriched in the “neutrophil activation” and “platelet activation pathways” at 4 dpf and in the “neutrophil apoptosis”, “ferroptosis”, and “necroptosis” pathways at 7 dpf. Conclusion Tritiated water exposure induces a temporally dynamic immune response in zebrafish, potentially affecting immune homeostasis by regulating neutrophil activation and apoptosis, as well as the expression of NF-κB and NLRP3.

Objective:To investigate the protective mechanism of cerium oxide nanoparticles(CeO2 NPs)against acute pancreatitis(AP),with a focus on their antioxidant and anti-inflammatory properties.Methods:CeO2 NPs were characterized by transmission elec-tron microscopy(TEM)and dynamic light scattering.In in vitro experiments,cell counting Kit-8(CCK-8)assay,flow cytometry,and Western blotting were used to validate the role of CeO2 NPs in preventing the apoptosis of pancreatic acinar cells.In in vivo experi-ments,C57BL/6 mice were divided into control group,AP group,AP+CeO2 group,SAP group,and SAP+CeO2 group to investigate the mechanism of action of CeO2 NPs in alleviating inflammation and oxidative stress in AP mice.Results:CeO2 NPs demonstrated rela-tively good stability and biocompatibility,with a particle size of(50±4)nm on TEM.In vitro experiments showed that CeO2 NPs sig-nificantly reduced the apoptosis of pancreatic acinar cells by alleviating lipid peroxidation and maintaining mitochondrial membrane potential.In vivo experiments showed that CeO2 NPs could reduce the serum levels of amylase,lipase,and inflammatory cytokines(in-terleukin-6 and tumor necrosis factor-α).This result might be related to the regulation of the IKK/P53/Bcl-2 pathway.CeO2 NPs re-duced the production of reactive oxygen species and enhanced anti-oxidant response by regulating the Nrf-2 signaling pathway.Con-clusion:CeO2 NPs exert anti-inflammatory and antioxidant effects by regulating the IκB kinase/tumor protein p53/B-cell lymphoma 2(IKK/P53/bcl-2)and nuclear factor erythroid 2-related(Nrf-2)signaling pathways,thereby showing promising potential for the treatment of AP.

Objective To explore the quantitative electroencephalography(qEEG)characteristics of the prefrontal cortex in patients with mild cognitive impairment(MCI)during digital screening tasks for MCI screening.Methods A total of 592 MCI patients(MCI group)and 317 normal cognitively elderly individuals(control group)were recruited from 40 communities in Nanjing,Jiangsu Province,from July to August,2024.All participants were as-sessed using Montreal Cognitive Assessment-Beijing Version(MoCA-BJ).Prefrontal EEG data were collected using a portable EEG device,and power spectral analysis was performed via Fast Fourier Transform.An XG-Boost algorithm was employed to construct an MCI identification model based on qEEG power features,and the model's performance was evaluated using receiver operating characteristic(ROC)curve.Results Compared with the control group,prefrontal δ,α,and β band power increased during screening tasks in MCI group(P<0.05);δ power was negatively correlated with MoCA-BJ total scores,and visuospatial/executive func-tion,attention and delayed recall scores(r=-0.269,-0.169,-0.133,-0.171,P<0.001);α power was negative-ly correlated with MoCA-BJ total scores,attention and delayed recall scores(r=-0.113,-0.075,-0.091,P<0.05).The XGBoost model based on δ and α power was excellent in MCI identification,with an area under the curve of 0.91,accuracy of 0.81,precision of 0.89,F1 score of 0.84,recall of 0.80,and specificity of 0.81.Conclusion MCI patients exhibit increased power in the prefrontal δ and α frequency bands during digital screening tasks,which is associated with cognitive decline.An XGBoost model based on qEEG power features can enable early prediction of MCI.

Objective To explore the quantitative electroencephalography(qEEG)characteristics of the prefrontal cortex in patients with mild cognitive impairment(MCI)during digital screening tasks for MCI screening.Methods A total of 592 MCI patients(MCI group)and 317 normal cognitively elderly individuals(control group)were recruited from 40 communities in Nanjing,Jiangsu Province,from July to August,2024.All participants were as-sessed using Montreal Cognitive Assessment-Beijing Version(MoCA-BJ).Prefrontal EEG data were collected using a portable EEG device,and power spectral analysis was performed via Fast Fourier Transform.An XG-Boost algorithm was employed to construct an MCI identification model based on qEEG power features,and the model's performance was evaluated using receiver operating characteristic(ROC)curve.Results Compared with the control group,prefrontal δ,α,and β band power increased during screening tasks in MCI group(P<0.05);δ power was negatively correlated with MoCA-BJ total scores,and visuospatial/executive func-tion,attention and delayed recall scores(r=-0.269,-0.169,-0.133,-0.171,P<0.001);α power was negative-ly correlated with MoCA-BJ total scores,attention and delayed recall scores(r=-0.113,-0.075,-0.091,P<0.05).The XGBoost model based on δ and α power was excellent in MCI identification,with an area under the curve of 0.91,accuracy of 0.81,precision of 0.89,F1 score of 0.84,recall of 0.80,and specificity of 0.81.Conclusion MCI patients exhibit increased power in the prefrontal δ and α frequency bands during digital screening tasks,which is associated with cognitive decline.An XGBoost model based on qEEG power features can enable early prediction of MCI.

Objective To explore the causal relationship between family resilience and mental health in military personnel population.Methods A total of 204 military personnel were recruited from an army unit stationed in Western China with cluster convenience sampling.Family Resilience Scale(FRS)and Symptom Checklist 90(SCL-90)were used to survey them twice,in an interval of 4 months.Amos 26.0 was applied to construct a cross-lag model and analyze the data.Results After controlling mental symptoms from the first survey,family resilience in the first measure significantly predicted mental symptoms in the second measure(β=-0.14,P＜0.05).After controlling for family resilience from the first survey,mental symptoms in the first measure significantly predicted family resilience in the second measure(β=-0.13,P＜0.05).Conclusion The relationship between family resilience and mental health is mutually causal in military personnel,and one predicts the other one.Our findings highlight the key dimensions of the relationship between the two.

An elderly female melanoma patient who experienced severe liver injury after treatment with pembrolizumab and axitinib,which improved with glucocorticoid therapy.Through medication analysis and adverse reaction scale evaluated,it was considered that severe liver injury was more closely related to the immune checkpoint inhibitor,pembrolizumab.After a comprehensive analysis of the relationship between liver injury and immunotherapy,as well as the benefits and risks of immunotherapy for patients,immunotherapy was rechallenged 40 days after discontinuation of pembrolizumab.Restarting treatment with pembrolizumab after immune-mediated hepatitis poses a risk of recurrence of hepatotoxicity.After reviewing related literature,it had been found that the incidence of severe hepatotoxicity caused by rechallenging treatment was low,and the overall safety was controllable.Pembrolizumab had brought therapeutic benefits to patients,with no further immune-mediated liver injury of 5 cycles medication.This case can provide a reference for rechallenging immunotherapy after immune-mediated hepatitis.

Nonalcoholic fatty liver disease （NAFLD） has gradually become the main reason affecting human liver health， and many factors are involved in the development and progression of NAFLD. Mitochondria， as the “energy factory” of cells， plays an important role in maintaining normal physiological functions. Studies have shown that hepatic mitochondrial dysfunction promotes the development and progression of NAFLD. This article briefly introduces the latest research advances in the basic characteristics and physiological function of liver mitochondria and reviews new research findings in the association of mitochondrial dysfunction with obesity， simple fatty liver disease， and nonalcoholic steatohepatitis， in order to provide new ideas for the research on targeted mitochondrial therapy for NAFLD.