Chronic obstructive pulmonary disease （COPD） is a respiratory disease characterized by airflow limitation， and its high morbidity and disability rates pose a severe challenge to global public health. Traditional Chinese medicine （TCM） has demonstrated definite efficacy and distinctive characteristics in the treatment of COPD. Based on the understanding of ancient and modern physicians regarding the etiology， pathogenesis， and stage-based syndrome differentiation of COPD， this article systematically elaborates on the etiology， pathogenesis， and clinical principles of syndrome differentiation and treatment of COPD. COPD is characterized by deficiency at root and excess in manifestation， with the coexistence of deficiency and excess. Qi deficiency is the fundamental pathogenesis underlying the occurrence and development of COPD and runs throughout the entire disease course. The disease begins with deficiency of lung qi and gradually affects the spleen and kidney， leading to the internal generation of dampness， phlegm， and blood stasis. Phlegm and blood stasis are not only pathological products but also deep-rooted causes of recurrent disease. Together with qi deficiency， they are mutually causal and form a vicious cycle. During the acute exacerbation stage of COPD， phlegm and blood stasis constitute the predominant underlying pathology and are often induced by invasion of pathogenic factors due to deficiency of healthy Qi. In addition， innovative understandings of the etiology and pathogenesis of COPD have emerged from the perspectives of collateral disease， latent pathogens， smoke toxins， and dysfunction of the Shaoyang pivot. During the stable stage， deficiency of Qi in the lung， spleen， and kidney predominates and is often accompanied by phlegm and blood stasis. In the clinical differentiation and treatment of COPD， treatment should be based on different disease stages and syndrome characteristics. During the acute exacerbation stage， eliminating pathogenic factors is the primary principle， with treatment determined according to syndrome differentiation. For wind-cold attacking the lung， the treatment is to ventilate the lung， disperse cold， and relieve cough. For phlegm-dampness accumulating in the lung， the treatment is to dry dampness， resolve phlegm， and direct qi downward. For phlegm-heat obstructing the lung， the treatment is to clear the lung， resolve phlegm， and relieve asthma. For phlegm and blood stasis obstructing the lung， the treatment is to eliminate phlegm， remove blood stasis， and relieve asthma. During the stable stage， reinforcing healthy Qi is the key principle. For lung-spleen qi deficiency， the treatment is to tonify the lung and strengthen the spleen， resolve phlegm， and direct Qi downward to relieve asthma. For deficiency of both lung and kidney， the treatment is to tonify the lung and benefit the kidney， resolve phlegm， promote Qi reception， and relieve asthma. When accompanied by phlegm and blood stasis， the treatment should focus on tonifying deficiency， resolving phlegm， and removing blood stasis. This article aims to systematically summarize the TCM etiology， pathogenesis， syndrome differentiation and treatment principles of COPD， as well as the current shortcomings in related research， in order to provide a reference for the clinical treatment of COPD with TCM， give full play to the advantages of TCM in the prevention and treatment of COPD， and optimize the whole-course management of COPD.

Chronic obstructive pulmonary disease （COPD） is a respiratory disease characterized by airflow limitation， and its high morbidity and disability rates pose a severe challenge to global public health. Traditional Chinese medicine （TCM） has demonstrated definite efficacy and distinctive characteristics in the treatment of COPD. Based on the understanding of ancient and modern physicians regarding the etiology， pathogenesis， and stage-based syndrome differentiation of COPD， this article systematically elaborates on the etiology， pathogenesis， and clinical principles of syndrome differentiation and treatment of COPD. COPD is characterized by deficiency at root and excess in manifestation， with the coexistence of deficiency and excess. Qi deficiency is the fundamental pathogenesis underlying the occurrence and development of COPD and runs throughout the entire disease course. The disease begins with deficiency of lung qi and gradually affects the spleen and kidney， leading to the internal generation of dampness， phlegm， and blood stasis. Phlegm and blood stasis are not only pathological products but also deep-rooted causes of recurrent disease. Together with qi deficiency， they are mutually causal and form a vicious cycle. During the acute exacerbation stage of COPD， phlegm and blood stasis constitute the predominant underlying pathology and are often induced by invasion of pathogenic factors due to deficiency of healthy Qi. In addition， innovative understandings of the etiology and pathogenesis of COPD have emerged from the perspectives of collateral disease， latent pathogens， smoke toxins， and dysfunction of the Shaoyang pivot. During the stable stage， deficiency of Qi in the lung， spleen， and kidney predominates and is often accompanied by phlegm and blood stasis. In the clinical differentiation and treatment of COPD， treatment should be based on different disease stages and syndrome characteristics. During the acute exacerbation stage， eliminating pathogenic factors is the primary principle， with treatment determined according to syndrome differentiation. For wind-cold attacking the lung， the treatment is to ventilate the lung， disperse cold， and relieve cough. For phlegm-dampness accumulating in the lung， the treatment is to dry dampness， resolve phlegm， and direct qi downward. For phlegm-heat obstructing the lung， the treatment is to clear the lung， resolve phlegm， and relieve asthma. For phlegm and blood stasis obstructing the lung， the treatment is to eliminate phlegm， remove blood stasis， and relieve asthma. During the stable stage， reinforcing healthy Qi is the key principle. For lung-spleen qi deficiency， the treatment is to tonify the lung and strengthen the spleen， resolve phlegm， and direct Qi downward to relieve asthma. For deficiency of both lung and kidney， the treatment is to tonify the lung and benefit the kidney， resolve phlegm， promote Qi reception， and relieve asthma. When accompanied by phlegm and blood stasis， the treatment should focus on tonifying deficiency， resolving phlegm， and removing blood stasis. This article aims to systematically summarize the TCM etiology， pathogenesis， syndrome differentiation and treatment principles of COPD， as well as the current shortcomings in related research， in order to provide a reference for the clinical treatment of COPD with TCM， give full play to the advantages of TCM in the prevention and treatment of COPD， and optimize the whole-course management of COPD.

Middle compartment defects,a common subtype of pelvic floor dysfunction(PFD),are primarily characterized by the prolapse of the uterus or vaginal vault.Magnetic resonance imaging(MRI)has emerged as a valuable diagnostic tool for PFD,offering superior soft tissue resolution while eliminating exposure to ionizing radiation.This review comprehensive summarizes current applications of MRI in the diagnosis and treatment of PFD,covering measurement methods,manifestations of three-level structural defects,postoperative efficacy evaluation,vaginal axial assessment,and evaluation of the mesh status.The authors suggest that MRI enables precise preoperative evaluation of three-level defects,thereby facilitating the development of personalized treatment plans.Additionally,MRI provides an accurate postoperative assessment of surgical outcomes and mesh status,offering a new basis for postoperative assessment.MRI demonstrates unique value in the diagnosis and treatment of middle compartment defects.

Objective To investigate the effects of Shenqi Tiaoshen Formula(SQTSF)for alleviating airway inflammation in rats with both chronic obstructive pulmonary disease(COPD)and lung-kidney qi deficiency syndrome and explore its therapeutic mechanism.Methods Forty-eight SD rats were randomly divided into control group,model group,low-,medium-,and high-dose SQTSF groups,and aminophylline(APL)group.In all but the control group,rat models of COPD with lung-kidney qi deficiency syndrome were established and treated with saline,SQTSF or APL via daily gavage as indicated(starting from day 30).The rats were observed for changes in body weight,grip strength,lung function,lung pathology,inflammatory cytokines in bronchoalveolar lavage fluid(BALF),oxidative stress levels,iron ion metabolism,cellular and mitochondrial ultrastructural changes in the lung tissue,and expressions of Nrf2/SLC7A11/GPX4 signaling pathway and ferroptosis-related proteins.Results The rats in the model group exhibited obvious symptoms of lung-kidney qi deficiency syndrome with significantly decreased body weight,grip strength,and lung function parameters.Examination of the lung tissue revealed showed significant inflammatory cell infiltration and emphysema with obvious bronchial,perivascular,and alveolar inflammation and alveolar destruction,significantly increased IL-1β,TNF-α,IL-6,and IL-13 levels in BALF,and elevated pulmonary oxidative stress levels and Fe2+and total iron ion concentrations.The rat models also showed characteristic ultrastructural changes of ferroptosis in the lung tissue cells under transmission electron microscope and significantly decreased Nrf2,GPX4,and SLC7A11 and increased ACSL4 expressions in the lung tissue.Treatment with SQTSF significantly improved these pathological changes in the rat models with a better effect than APL.Conclusion SQTSF can effectively improve airway inflammation and oxidative stress in COPD rats with lung-kidney qi deficiency possibly by inhibiting ferroptosis via regulating the Nrf2/SLC7A11/GPX4 signaling pathway.

Pharmacological perturbation studies based on protein-level signatures are fundamental for drug dis-covery.In the present study,we used a mass spectrometry(MS)-based proteomic platform to profile the whole proteome of the breast cancer MCF7 cell line under stress induced by 78 bioactive compounds.The integrated analysis of perturbed signal abundance revealed the connectivity between phenotypic behaviors and molecular features in cancer cells.Our data showed functional relevance in exploring the novel pharmacological activity of phenolic xanthohumol,as well as the noncanonical targets of clinically approved tamoxifen,lovastatin,and their derivatives.Furthermore,the rational design of synergistic inhibition using a combination of histone methyltransferase and topoisomerase was identified based on their complementary drug fingerprints.This study provides rich resources for the proteomic landscape of drug responses for precision therapeutic medicine.

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Objective To investigate the effects of Shenqi Tiaoshen Formula(SQTSF)for alleviating airway inflammation in rats with both chronic obstructive pulmonary disease(COPD)and lung-kidney qi deficiency syndrome and explore its therapeutic mechanism.Methods Forty-eight SD rats were randomly divided into control group,model group,low-,medium-,and high-dose SQTSF groups,and aminophylline(APL)group.In all but the control group,rat models of COPD with lung-kidney qi deficiency syndrome were established and treated with saline,SQTSF or APL via daily gavage as indicated(starting from day 30).The rats were observed for changes in body weight,grip strength,lung function,lung pathology,inflammatory cytokines in bronchoalveolar lavage fluid(BALF),oxidative stress levels,iron ion metabolism,cellular and mitochondrial ultrastructural changes in the lung tissue,and expressions of Nrf2/SLC7A11/GPX4 signaling pathway and ferroptosis-related proteins.Results The rats in the model group exhibited obvious symptoms of lung-kidney qi deficiency syndrome with significantly decreased body weight,grip strength,and lung function parameters.Examination of the lung tissue revealed showed significant inflammatory cell infiltration and emphysema with obvious bronchial,perivascular,and alveolar inflammation and alveolar destruction,significantly increased IL-1β,TNF-α,IL-6,and IL-13 levels in BALF,and elevated pulmonary oxidative stress levels and Fe2+and total iron ion concentrations.The rat models also showed characteristic ultrastructural changes of ferroptosis in the lung tissue cells under transmission electron microscope and significantly decreased Nrf2,GPX4,and SLC7A11 and increased ACSL4 expressions in the lung tissue.Treatment with SQTSF significantly improved these pathological changes in the rat models with a better effect than APL.Conclusion SQTSF can effectively improve airway inflammation and oxidative stress in COPD rats with lung-kidney qi deficiency possibly by inhibiting ferroptosis via regulating the Nrf2/SLC7A11/GPX4 signaling pathway.

Objective:To explore the value of the aMAP risk score (age, male, albumin -bilirubin, and platelets) to predict early recurrence within one year after microwave ablation in patients with small hepatocellular carcinoma. Methods:This was a retrospective study that enrolled 142 patients diagnosed with hepatocellular carcinoma who were treated with microwave ablation in the Department of Hepatology Unit of Nanfang Hospital, Southern Medical University from July 2016 to July 2021. The cohort enrolled 121 male and 21 female patients, including 110 patients that were <60 years old. All the patients were followed-up after microwave ablation to evaluate residual tumor and recurrence of tumor by computed tomography or magnetic resonance imaging. The observation indices mainly included general data and imaging data of patients. Using the X-tile tools, patients were divided into two groups: a high aMAP score group and a low aMAP score group. Multivariate Cox regression analysis was conducted for comparison of independent risk factors.Results:Multivariate Cox regression showed that high aMAP score, maximum tumor diameter >20 mm, and high AFP were the independent risk factors of early recurrence (all P<0.05). Kaplan-Meier survival curves showed that the median recurrence-free survival was 25.5 months in the low aMAP score group and 6.1 months in the high aMAP score group ( P=0.001). Conclusions:The aMAP score could predict the early recurrence within 1 year of small hepatocellular carcinoma after microwave ablation. Patients with high aMAP score should undergo rigorous postoperative follow-up evaluations..

Objective:To study the effects of salivary microbiota in patients with periodontitis on the tryptophan-aryl hydrocarbon receptor (AhR) signaling axis in mice with periodontitis and to provide theoretical basis as well as new ideas for the influences of periodontitis on systemic metabolism.Methods:Salivary microbiota of 12 healthy individuals and 14 patients with periodontitis were collected in Nanjing Stomatological Hospital, Medical School of Nanjing University from June to December of 2020. According to the random number table method, twenty-four mice were randomly divided into three groups: Sham group (control group), P group (periodontitis patients′ salivary microbiota group) and H group (periodontal healthy individuals′ salivary microbiota group). The maxillary second molars of all mice were treated with silk thread ligation to induce periodontitis. Phosphate buffer as well as salivary microbiota of periodontal healthy individuals and periodontitis patients were gavaged into periodontitis mice for 2 weeks. The expression of inflammatory factors in mice serum were detected by enzyme linked immunosorbent assay, and the expression of tryptophan and indole metabolites in intestinal tract and serum were detected by liquid chromatography-mass spectrometry. The expression of AhR in intestinal tract of mice was detected by immunohistochemistry and quantitative real time-PCR while gut microbiota constitution was detected by 16S rRNA gene sequencing. The remaining saliva samples of periodontitis patients and periodontal healthy individuals were applied to detect the expression of tryptophan and indole metabolites themselves.Results:The salivary microbiota of periodontitis patients could induce the expression of interleukin-1β [P group: (162.38±39.46) pg/ml, H group: (82.83±20.01) pg/ml; t=4.40, P=0.001) and tumor necrosis factor-α [P group: (361.16±123.90) pg/ml, H group: (191.66±106.87) pg/ml; t=2.54, P=0.030) in serum of periodontitis mice, and reduce the expression of AhR in colon (P group: 1.18±0.05, H group:1.83±0.47; t=3.09, P=0.015) and ileum (P group: 0.80±0.13, H group: 1.18±0.11; t=4.93, P=0.001). After gavage of salivary microbiota of periodontitis patients to the mice, tryptophan (P group: (18.1±3.8)×10 7, H group: (26.6±6.6)×10 7; t=2.49, P=0.037] and indole lactic acid [P group: (1.9±0.7)×10 7, H group: (3.7±0.6)×10 7; t=4.49, P=0.002) in serum of periodontitis mice were significantly decreased, but was relatively disorder in intestinal tract. However, the expressions of tryptophan and indole metabolites in saliva of periodontitis patients were higher than those of periodontal healthy individuals. There were significant differences in indole propionic acid [P group: (1 239.39±818.72) nmol/L, H group: (56.96±38.33) nmol/L; t=2.83, P=0.022]. What we find noteworthy was that the expressions of indolelactic acid metabolism in saliva, serum and intestinal were consistent, and salivary microbiota of periodontitis patients could reduce the relative abundance of indolelactic acid-producing bacteria in the gut, suggesting that the salivary microbiota of periodontitis patients might affect the expression of AhR through gut microbiota disorder and indolelactic acid downregulation. Conclusions:Salivary microbiota in patients with periodontitis may affect the systemic inflammatory state through down-regulating the expression of tryptophan-AhR signal axis.

Objective:To investigate the consistency and diagnostic efficiency of Chinese Thyroid Imaging Reporting and Date System (C-TIRADS) in thyroid nodule evaluation by different seniority sonographers.Methods:The preoperative ultrasonographic datum of 134 thyroid nodules in 112 patients from January to November 2020 were independently analyzed by sonographers with different seniority. According to the C-TIRADS guidelines, the C-TIRADS ultrasonographic indicators of each nodule were recorded and C-TIRADS classification was performed. Cohen′s Kappa (K) statistical method was used to analyze the consistency of ultrasonic indicators evaluated by different seniority sonographers. Using postoperative pathological results as the gold standard, the diagnostic efficacy of C-TIRADS classification for differentiating benign and malignant thyroid nodules by junior and senior sonographers was calculated respectively, and the Receiver Operating Characteristic (ROC) curves were drawn respectively.Results:The solid structure and vertical orientation of thyroid nodule judged by different seniority sonographers were very consistent ( K=0.84, 0.81). The consistencies of very hypoechoic and microcalcifications were substantial agreement ( K=0.80, 0.61), and moderate ( K=0.531) for the margin of the nodules. The sensitivity, specificity, accuracy, positive predictive value and negative predictive value of distinguishing benign and malignant thyroid nodules by junior and senior sonographers were 91.8%, 65.8%, 77.6%, 69.1%, 90.6% and 96.7%, 67.1%, 80.6%, 71.1%, 96.1%, respectively. The corresponding area under the ROC curves were 0.788 and 0.819, respectively ( Z=1.369, P=0.171). Conclusion:Ultrasonologists with different experience have good consistency in evaluating the C-TIRADS ultrasonic indicators of thyroid nodule, and the diagnostic efficacy of C-TIRADS classification in differentiating benign and malignant thyroid nodule was similar.