Diabetic cardiomyopathy （DCM） is one of the most common complications of diabetes mellitus and is a major threat to global health. As a key mechanism in the occurrence and progression of DCM， the inflammatory response persists throughout the entire course of the DCM. The Gaozhuo theory suggests that the basic pathogenesis of inflammatory injury in DCM is the Qi deficiency of spleen and kidney and Gaozhuo invasion， and divides the pathological process into three phases： Gaozhuo invasion， turbid heat damage to the channels， and turbid blood stasis and heat junction. Among them， the Qi deficiency of spleen and kidney and the endogenous formation of Gaozhuo represent the process of inflammatory factor formation induced by glucose metabolism disorders. Turbid heat damage to the channels refers to the process of myocardial inflammatory injury mediated by inflammatory factors， and turbid blood stasis and heat junction are the process of myocardial injury developing toward myocardial fibrosis and ventricular remodeling. As the disease continues to progress， it eventually develops into a depletion of the heart Yang， leading to the ultimate regression of heart failure. According to the theory of Gaozhuo， traditional Chinese medicine （TCM） should regulate inflammatory injury in DCM by strengthening the spleen and tonifying the kidney to address the root cause， and resolving dampness and lowering turbidity to treat the symptoms. If the turbidity has been stored for a long time and turns into heat， strengthening the spleen and tonifying the kidney， and clearing heat and resolving turbidity should be the therapy. If the turbidity， stasis， and heat are knotted in the heart and collaterals， strengthening the spleen and tonifying the kidney， and resolving stasis and lowering turbidity should be the therapy. TCM compounds and monomers can regulate the inflammatory response in DCM. TCM compounds can be divided into the categories for benefiting Qi to resolve turbidity， benefiting Qi and clearing heat to resolve turbidity， and benefiting Qi and activating blood to reduce turbidity. The compounds can inhibit upstream signals of inflammation and expression of inflammatory factors， improve the inflammatory damage to myocardium and blood vessels， myocardial fibrosis， and cardiac systole and diastole， and thus slow down the onset and progression of DCM.

Interferon regulatory factor 4 (IRF4) is a critical transcription factor that governs the differentiation of cluster of differentiation 4⁺ (CD4⁺) T cells. The pathogenesis and progression of psoriasis are primarily attributed to an immune imbalance stemming from the overproduction of interleukin-17A (IL-17A) by T lymphocytes. However, the role of IRF4 in psoriasis remains unexplored. In this study, we found that IRF4 activity is increased in the cutaneous lesions of patients with psoriasis in response to stimulation by IL-23A and IL-1β. This IRF4 elevation heightens its binding to the E1A binding protein p300 (EP300) promoter, triggering the transcription of downstream retinoic acid receptor-related orphan receptor-γt (RORγt) and increasing the secretion of IL-17A, thereby establishing the IL-1β/IL-23A-IRF4-EP300-RORC-IL-17A inflammatory cascade in psoriasis. The alleviation of imiquimod (IMQ)-induced psoriatic-like symptoms was achieved through the creation of a Irf4 ^-/- gene deletion mouse model and pharmacological inhibition using antisense oligonucleotides targeted for Irf4. This amelioration was accompanied by a decreased number of IL-17A-producing CD4⁺ T cells in the skin. The findings of this study suggest that IRF4 plays a crucial role in the promotion of inflammation and exacerbation of IMQ-induced psoriasiform dermatitis. Consequently, IRF4 targeting could be a promising therapeutic strategy.

For middle-aged and elderly patients with conditions such as spinal fractures and degenerative spinal diseases, spinal internal fixation is a core surgical procedure for reconstructing spinal stability, heavily relying on the biomechanical stability provided by pedicle screw systems. Whereas, these patients are often complicated by osteoporosis that can significantly compromise the stability of the bone-pedicle screw interface, leading to a marked increase in pedicle screw loosening and surgical failure rates. The bone cement-augmented pedicle screw technique, which involves injecting bone cement into the vertebral body or screw trajectory to optimize the mechanical properties of the bone-pedicle screw composite, has been proven to significantly enhance fixation strength and effectively prevent screw-related failures, thereby reducing the incidence of internal fixation failure in high-risk populations undergoing spinal fusion. However, the widespread clinical application of this technique has faced challenges such as inaccurate clinical decision-making (indication and contraindication selection), non-standardized operative practices, and insufficient awareness of complication prevention, resulting in considerable variability in clinical outcomes and even severe complications. To address this, Prof. Luo Fei from First Affiliated Hospital of Army Medical University initiated the project and the Chinese Association Orthopaedic Surgeons organized relevant experts to develop the Evidence-based clinical practice guideline for bone cement-augmented pedicle screw technique ( version 2025), based on current evidence. The guidelines put forward 8 recommendations regarding the clinical value, scope of application, and operational standards of the technique, aiming to provide evidence-based medical support and technical standardization for clinical decision-making.

Objective To investigate the association of serum exosomal microRNAs(miRNAs)with hepatic inflammatory injury and histological outcomes in patients with chronic hepatitis B(CHB).Methods Peripheral serum samples were collected from six healthy adults and six patients with CHB,and size exclusion chromatography was used to extract exosomes.Small RNA sequencing and transcriptomic analysis were used to identify the serum exosomal miRNAs associated with liver inflammatory injury and fibrosis,and quantitative real-time PCR was used for validation in a mouse model of acute liver injury induced by lipopolysaccharide/D-galactosamine,a rat model of liver fibrosis induced by carbon tetrachloride,and 84 CHB patients undergoing liver biopsy twice before and after treatment.The independent-samples t test was used for comparison of normally distributed continuous data between two groups;an analysis of variance was used for comparison between multiple groups,and the Tukey test was used for further comparison between two groups.The Mann-Whitney U test was used for comparison of non-normally distributed continuous data between two groups;the Kruskal-Wallis H test was used for comparison between multiple groups,and the Dunn test was used for further comparison between two groups.The chi-square test or the Fisher's exact test was used for comparison of categorical data between groups.The univariate and multivariate Logistic regression analyses were used to investigate influencing factors.Results Abnormal expression of serum exosomal miR-122-5p was observed in patients with CHB,and it was downregulated in patients with confluent necrosis and advanced fibrosis.In the mouse model of acute liver injury and the rat model of liver fibrosis,compared with the control group,the model group had a significant reduction in the expression level of miR-122-5p in the liver(P=0.048 and 0.014),and compared with the patients with mild liver injury,the patients with severe confluent necrosis and advanced fibrosis showed a significant reduction in the expression level of miR-122-5p in liver tissue(P<0.05).Among the 84 CHB patients,the patients with severe hepatic confluent necrosis or advanced liver fibrosis had a significantly lower expression level of serum exosomal miR-122-5p than those with mild liver injury(P<0.001 and P=0.003).The multivariate Logistic regression analysis showed that the expression level of miR-122-5p was an independent influencing factor for confluent necrosis(odds ratio[OR]=0.001,95%confidence interval[CI]:0.000-0.037,P=0.005)and liver fibrosis degree(OR=0.568,95%CI:0.331-0.856,P=0.019).In addition,compared with the patients with low expression of miR-122-5p,the patients with high expression of miR-122-5p before treatment had a significantly higher reversal rate of liver fibrosis after 72 weeks of antiviral therapy(64.3%vs 38.1%,P=0.029).Conclusion Serum exosomal miR-122-5p in CHB patients is closely associated with the progression of hepatic confluent necrosis and fibrosis,and the reduction in the expression level of miR-122-5p may aggravate hepatic confluent necrosis,promote the progression of fibrosis,and affect the histological outcome of CHB patients after antiviral therapy.

ObjectiveTo investigate the association of serum exosomal microRNAs （miRNAs） with hepatic inflammatory injury and histological outcomes in patients with chronic hepatitis B （CHB）. MethodsPeripheral serum samples were collected from six healthy adults and six patients with CHB， and size exclusion chromatography was used to extract exosomes. Small RNA sequencing and transcriptomic analysis were used to identify the serum exosomal miRNAs associated with liver inflammatory injury and fibrosis， and quantitative real-time PCR was used for validation in a mouse model of acute liver injury induced by lipopolysaccharide/D-galactosamine， a rat model of liver fibrosis induced by carbon tetrachloride， and 84 CHB patients undergoing liver biopsy twice before and after treatment. The independent-samples t test was used for comparison of normally distributed continuous data between two groups； an analysis of variance was used for comparison between multiple groups， and the Tukey test was used for further comparison between two groups. The Mann-Whitney U test was used for comparison of non-normally distributed continuous data between two groups； the Kruskal-Wallis H test was used for comparison between multiple groups， and the Dunn test was used for further comparison between two groups. The chi-square test or the Fisher’s exact test was used for comparison of categorical data between groups. The univariate and multivariate Logistic regression analyses were used to investigate influencing factors. ResultsAbnormal expression of serum exosomal miR-122-5p was observed in patients with CHB， and it was downregulated in patients with confluent necrosis and advanced fibrosis. In the mouse model of acute liver injury and the rat model of liver fibrosis， compared with the control group， the model group had a significant reduction in the expression level of miR-122-5p in the liver （P=0.048 and 0.014）， and compared with the patients with mild liver injury， the patients with severe confluent necrosis and advanced fibrosis showed a significant reduction in the expression level of miR-122-5p in liver tissue （P<0.05）. Among the 84 CHB patients， the patients with severe hepatic confluent necrosis or advanced liver fibrosis had a significantly lower expression level of serum exosomal miR-122-5p than those with mild liver injury （P<0.001 and P=0.003）. The multivariate Logistic regression analysis showed that the expression level of miR-122-5p was an independent influencing factor for confluent necrosis （odds ratio ［OR］=0.001， 95% confidence interval ［CI］： 0.000‍ ‍—‍ ‍0.037， P=0.005） and liver fibrosis degree （OR=0.568， 95%CI： 0.331‍ ‍—‍ ‍0.856， P=0.019）. In addition， compared with the patients with low expression of miR-122-5p， the patients with high expression of miR-122-5p before treatment had a significantly higher reversal rate of liver fibrosis after 72 weeks of antiviral therapy （64.3% vs 38.1%， P=0.029）. ConclusionSerum exosomal miR-122-5p in CHB patients is closely associated with the progression of hepatic confluent necrosis and fibrosis， and the reduction in the expression level of miR-122-5p may aggravate hepatic confluent necrosis， promote the progression of fibrosis， and affect the histological outcome of CHB patients after antiviral therapy.

For middle-aged and elderly patients with conditions such as spinal fractures and degenerative spinal diseases, spinal internal fixation is a core surgical procedure for reconstructing spinal stability, heavily relying on the biomechanical stability provided by pedicle screw systems. Whereas, these patients are often complicated by osteoporosis that can significantly compromise the stability of the bone-pedicle screw interface, leading to a marked increase in pedicle screw loosening and surgical failure rates. The bone cement-augmented pedicle screw technique, which involves injecting bone cement into the vertebral body or screw trajectory to optimize the mechanical properties of the bone-pedicle screw composite, has been proven to significantly enhance fixation strength and effectively prevent screw-related failures, thereby reducing the incidence of internal fixation failure in high-risk populations undergoing spinal fusion. However, the widespread clinical application of this technique has faced challenges such as inaccurate clinical decision-making (indication and contraindication selection), non-standardized operative practices, and insufficient awareness of complication prevention, resulting in considerable variability in clinical outcomes and even severe complications. To address this, Prof. Luo Fei from First Affiliated Hospital of Army Medical University initiated the project and the Chinese Association Orthopaedic Surgeons organized relevant experts to develop the Evidence-based clinical practice guideline for bone cement-augmented pedicle screw technique ( version 2025), based on current evidence. The guidelines put forward 8 recommendations regarding the clinical value, scope of application, and operational standards of the technique, aiming to provide evidence-based medical support and technical standardization for clinical decision-making.

Objective:To explore the effectiveness of 18F-deuterated-Florbetapir (D3FSP) PET/CT imaging in detecting β-amyloid (Aβ) deposition in the brain and its correlation with plasma biomarkers. Methods:A retrospective analysis was conducted on 79 patients (32 males, 47 females; age(66±7)years) who underwent 18F-D3FSP PET/CT imaging from June 2022 to November 2023 at the First Affiliated Hospital, Guangzhou Medical University, as a part of the Greater Bay Area Healthy Aging Brain Longitudinal Cohort Study (GHABS). Based on the Alzheimer′s Disease Neuroimaging Initiative cohort standard protocol, patients were categorized into cognitively unimpaired (CU) group, mild cognitive impairment (MCI) group, and Alzheimer′s disease (AD) group. Brain regions were segmented using the AW workstation and the SUV ratio (SUVR) was calculated with the cerebellum as the reference region. One-way analysis of variance, Bonferroni correction and Pearson correlation analysis were used to analyze data. The ROC curve analysis was used to analyze the cut-off value and the diagnostic efficacy of SUVR. Results:There were 48, 15 and 16 cases in CU, MCI and AD groups respectively. During the transition from CU to MCI and then to AD, there was a rising trend in SUVR ( F values: 11.15-22.38, all P<0.001) across the whole brain and various brain regions (bilateral frontal lobes, bilateral anterior cingulate gyrus, bilateral precuneus, bilateral parietal lobes, bilateral lateral temporal lobes, and bilateral occipital lobes). SUVRs of the right anterior cingulate gyrus and bilateral precuneus were different between the CU and MCI groups (all P<0.017), and those of bilateral frontal lobes, right precuneus, bilateral parietal lobes, bilateral lateral temporal lobes, and bilateral occipital lobes were different between the MCI and AD groups (all P<0.017). SUVRs of brain regions were negatively correlated with cognitive scale scores ( r values: from -0.57 to -0.37, all P<0.001), and were positively correlated with plasma phosphorylated tau181 (p-tau181, r values: 0.50-0.61, all P<0.001). The ROC curve analysis suggested that the cut-off value of SUVR in the precuneus for distinguishing CU from AD was 1.20, with the AUC, sensitivity, specificity and accuracy of 0.85, 12/16, 91.7%(44/48)and 87.5%(56/64), respectively. Conclusion:18F-D3FSP PET/CT imaging has good clinical application value in assessing the deposition sites and the extent of Aβ in the brain, which is related to clinical cognition and plasma p-tau181 level.

Objective:To explore the role and mechanism of nuclear factor erythroid 2-related factor 2 (NRF2) in lung injury in mice with Staphylococcus aureus-induced sepsis. Methods:A sepsis mouse model with Staphylococcus aureus infection was created using wild-type C57BL/6 male mice and NRF2 -/- male mice aged six to eight weeks. The mice were divided into four groups with five in each group. In WT control group and NRF2 -/- control group, the wild type mice and NRF2 -/- mice were intraperitoneally injected with 100 μL phosphate buffered saline (PBS) respectively. In WT model group and NRF2 -/- model group, the wild type mice and NRF2 -/- mice were intraperitoneally injected with 100 μL PBS containing Staphylococcus aureus (3×10 8 colony forming unit (CFU)/mL) respectively. The lung samples were taken under anesthesia six hours after injection, and hematoxylin and eosin staining was performed to observe tissuse lesions. The survival of the mice was evaluated. The protein concentrations and cell counts in the bronchoalveolar lavage fluid (BALF), the mRNA relative expressions of tumor necrosis factor-alpha (TNF-α), interleukin-6 (IL-6), and interleukin-1 beta (IL-1β) in lung tissues, and the serum levels of myeloperoxidase (MPO), malondialdehyde (MDA), and superoxide dismutase (SOD) were compared among the four groups. Independent samples t test was used for statistical comparison. Results:After six days of observation, no mice died in WT control group and NRF2 -/- control group, three mice died in WT model group on day 3, and four mice died in NRF2 -/- model group on day 4. The pathological staining showed that macrophage infiltration and alveolar structure damage occurred in the lung tissuse of WT model group, and the damage were more significant in NRF2 -/- model group. The protein concentrations and cell counts in BALF of mice in WT control group were (342±23) μg/mL and (5.78±2.67)×10 5/mL, respectively, those in WT model group were (657±39) μg/mL and (10.78±5.57)×10 5/mL, respectively, those in NRF2 -/- control group were (312±45) μg/mL and (5.67±1.46)×10 5/mL, respectively, and those in NRF2 -/- model group were (957±85) μg/mL and (13.85±3.72)×10 5/mL, respectively. The protein concentrations and cell counts in WT model group were higher than those in WT control group ( t=6.56, P<0.001 and t=8.21, P<0.001, respectively), while lower than NRF2 -/- model group ( t=2.32, P=0.001 and t=3.11, P=0.002, respectively). The differences were all statistically significant. Compared with the WT model group, the mRNA relative expressions of TNF-α (4.345±1.131 vs 12.375±4.534), IL-1β (5.395±2.112 vs 6.865±2.185), IL-6 (2.964±0.945 vs 5.467±1.855) in the lung tissues of NRF2 -/- model group increased, and the serum levels of MPO (2.956±1.211 vs 4.745±1.945) and MDA (4.333±1.652 vs 8.234±3.734) increased, while the level of SOD (17.121±8.183 vs 11.967±8.122) decreased, with statistically differences ( t=1.77, 4.67, 2.99, 7.99, 10.45 and 8.45, respectively, all P<0.05). Conclusions:The absence of NRF2 gene can exacerbate the inflammatory response and oxidative stress in mice with Staphylococcus aureus-induced sepsis, leading to more severe lung tissue damage.

Objective:To analyze the efficacy of anterior cervical Hybrid surgery and posterior cervical expansive open-door laminoplasty(EODL)in the treatment of multilevel cervical spondylotic myelopathy,and to discuss the selection of surgical methods for the patients with multilevel cervical spondylotic myelopathy.Methods:The retrospective analysis was conducted of 70 patients with multilevel cervical spondylotic myelopathy who underwent surgery at Affilated Beijing Traditional Chinese Medicine Hospital of Capital Medical University from July 2017 to July 2020.Based on the different surgical methods,the patients were divided into anterior group(n=35)and posterior group(n=35).The patients in anterior group underwent Hybrid surgery[anterior cervical discectomy and fusion(ACDF)combined with artificial cervical disc replacement(ACDR)],and the patients in posterior group underwent EODL.The hospitalization time,operation time,intraoperative blood loss,and postoperative drainage volume of the patients in two groups were recorded;the efficacy was evaluated by Japanese orthopaedic association(JOA)score,JOA improvement rate,neck disability index(NDI),visual analogue scale(VAS)for pain,and postoperative satisfaction score;the complications of the patients in two groups after surgery were recorded.Results:Compared with posterior group,the intraoperative blood loss,postoperative drainage volume,hospitalization time,and operation time of the patients in anterior group were significantly decreased(P<0.01),and the preoperative score had no significant difference(P>0.05).At the final follow-up after surgery,compared with posterior group,the JOA score and JOA improvement rate of the patients in anterior group were significantly increased(P<0.01),and the NDI score and VAS score were significantly decreased(P<0.01).Compared with before surgery,the JOA scores of the patients in two groups at the final follow-up after surgery were increased(P<0.01),and the NDI and VAS scores were significant decreased(P<0.01).The postoperative satisfaction of the patients in two groups was high based on the postoperative satisfaction score.There was no significant difference in the incidence of postoperative complication of the patients between two groups(P>0.05).Conclusion:Both the anterior cervical Hybrid surgery and EODL achieve the satisfactory results in the treatment of multilevel cervical spondylotic myelopathy.Hybrid surgery has the advantages of less bleeding and shorter surgery time,and the most suitable surgical method should be chosen clinically based on the actual situation of the patients.

Objective:To explore the correlation between c-myc and glutaminase(GLS)and glutamine synthase(GS)in oral epider-moid carcinoma cells in animal models.Methods:Immunohistochemistry was used to detect the expression of c-myc,GLS and GS in clinical samples of oral cancer.KB cell model with stable and high expression of c-myc was established and verified,then the KB cells were transplanted into nude mice to establish mouse tumorigenic models.The cells and nude mouse models were respectively diveded into 3 groups(n=6):normal cotnrol,empty vector and c-myc overexpression groups.The tumor growth was observed.The expression of c-myc,GLS and GS in the cells and the tumor samples was detected by immunohistochemistry.Results:c-myc,GLS and GS were highly expressed in clinical samples of oral cancer.In the cells of c-myc overexpression group c-myc mRNA expression level was sig-nificantly higher than that of empty vector control group.The tumorigenic models were formed in all nude mice of the groups,and the volume and weight of the c-myc overexpression group increased more significantly(P＜0.01),in the c-myc overexpression group c-myc was overexpressed,the expression of GLS and GS was significantly higher than that in the other 2 groups.Conclusion:c-myc is highly expressed in oral cancer,and may up-regulate GLS and GS expression.