ObjectiveTo investigate the intervention mechanism of the traditional Chinese medicine Number 2 Feibi recipe （N2FBR） in idiopathic pulmonary fibrosis （IPF）， focusing on its effects on endoplasmic reticulum （ER） stress， apoptosis， stemness maintenance， and regenerative capacity of alveolar type Ⅱ epithelial cells （AT2 cells）， and to validate the modern translational pathway of the theory of "deficiency of Zong Qi leading to pulmonary atelectasis and atrophy". MethodsA mouse model of pulmonary fibrosis was induced by bleomycin （BLM）. Mice were randomly divided into blank control， model， low-， and high-dose N2FBR intervention groups （9.1， 18.2 g·kg^-1）， and prednisolone intervention group （6.5 mg·kg^-1）. Pulmonary histopathological changes and collagen deposition were evaluated using hematoxylin-eosin （HE） and Masson's trichrome staining. Hydroxyproline （HYP） content was measured by the alkaline hydrolysis method. Lung coefficient and pulmonary function parameters were evaluated. The mRNA expression levels of fibrosis-related factors， including collagen type Ⅰ alpha 1 chain （ColIa1）， alpha-smooth muscle actin （α-SMA）， and tissue inhibitor of metalloproteinase 1 （Timp1）， were detected by real-time polymerase chain reaction （Real-time PCR）. Cell apoptosis was assessed using the terminal deoxynucleotidyl transferase dUTP nick-end labeling （TUNEL） assay. Apoptosis of AT2 cells was further evaluated by double immunofluorescence staining for surfactant protein C （SPC） and cysteine-aspartic protease-3 （Caspase-3）. Endoplasmic reticulum （ER） stress in AT2 cells was examined by double staining for SPC and protein kinase R-like endoplasmic reticulum kinase （PERK）. Ultrastructural changes of ER and lamellar bodies in AT2 cells were observed by transmission electron microscopy （TEM）. The expression levels of key proteins involved in ER stress and apoptosis pathways， including PERK， activating transcription factor 4 （ATF4）， and Caspase-3， were detected by Western blot. Double immunofluorescence staining of SPC and Ki-67 antigen （Ki-67） was performed to evaluate the proliferative capacity of AT2 cells. Lineage tracing technology （labeling AT2 cells with GFP） combined with Krt8 labeling was used to evaluate intermediate differentiation states， and morphological transformation of AT2 cells into alveolar type Ⅰ epithelial cells （AT1） was observed. ResultsBLM-induced mice exhibited significant structural disruption of lung tissue， increased collagen deposition， elevated lung coefficient， decreased pulmonary function， and upregulation of fibrosis-related factors （P<0.01）. High-dose N2FBR treatment significantly ameliorated lung tissue damage and dysfunction， significantly reduced HYP content （P<0.01）， and significantly downregulated ColIa1， α-SMA， and Timp1 expression （P<0.01）. Apoptosis analysis showed increased TUNEL-positive and Caspase-3-positive AT2 cells in the model group， which was significantly reduced by high-dose N2FBR treatment. TEM revealed swollen ER structures in AT2 cells of the model group， which tended to return to normal following treatment. PERK protein staining analysis showed evident ER stress in AT2 cells of the model group， which were markedly alleviated in the treatment group. The expression levels of ER stress-related proteins PERK and ATF4， as well as the apoptosis-related protein Caspase-3， were elevated in the model group and significantly reduced after treatment. TEM also revealed disrupted lamellar body structures in the model group， which tended to recover in the treatment group. Regarding the proliferative capacity of AT2 cells， the proportion of Ki-67⁺SPC⁺ AT2 cells significantly increased in the treatment group （P<0.01）. Lineage tracing showed that the proportion of keratin 8-positive green fluorescent protein-positive （Krt8⁺GFP⁺） cells increased in the model group， indicating differentiation arrest. This proportion was significantly reduced in the treatment group， and the morphology of GFP⁺ cells exhibited a flattened， extended shape， suggesting restored differentiation toward AT1 cells. ConclusionN2FBR alleviates ER stress in AT2 cells， reduces AT2 cell apoptosis， restores lamellar body structure and function， enhances proliferation activity， and alleviates differentiation arrest to promote differentiation into AT1 cells， thereby repairing the alveolar epithelium and effectively blocking the progression of pulmonary fibrosis. Its traditional Chinese medicine mechanism of "replenishing Zong Qi， harmonizing Qi and blood， and unblocking pulmonary meridians" closely aligns with the modern regulatory pathway of AT2 stem cells， providing a novel theoretical basis and experimental evidence for the intervention of IPF with traditional Chinese medicine.

ObjectiveTo investigate the intervention mechanism of the traditional Chinese medicine Number 2 Feibi recipe （N2FBR） in idiopathic pulmonary fibrosis （IPF）， focusing on its effects on endoplasmic reticulum （ER） stress， apoptosis， stemness maintenance， and regenerative capacity of alveolar type Ⅱ epithelial cells （AT2 cells）， and to validate the modern translational pathway of the theory of "deficiency of Zong Qi leading to pulmonary atelectasis and atrophy". MethodsA mouse model of pulmonary fibrosis was induced by bleomycin （BLM）. Mice were randomly divided into blank control， model， low-， and high-dose N2FBR intervention groups （9.1， 18.2 g·kg^-1）， and prednisolone intervention group （6.5 mg·kg^-1）. Pulmonary histopathological changes and collagen deposition were evaluated using hematoxylin-eosin （HE） and Masson's trichrome staining. Hydroxyproline （HYP） content was measured by the alkaline hydrolysis method. Lung coefficient and pulmonary function parameters were evaluated. The mRNA expression levels of fibrosis-related factors， including collagen type Ⅰ alpha 1 chain （ColIa1）， alpha-smooth muscle actin （α-SMA）， and tissue inhibitor of metalloproteinase 1 （Timp1）， were detected by real-time polymerase chain reaction （Real-time PCR）. Cell apoptosis was assessed using the terminal deoxynucleotidyl transferase dUTP nick-end labeling （TUNEL） assay. Apoptosis of AT2 cells was further evaluated by double immunofluorescence staining for surfactant protein C （SPC） and cysteine-aspartic protease-3 （Caspase-3）. Endoplasmic reticulum （ER） stress in AT2 cells was examined by double staining for SPC and protein kinase R-like endoplasmic reticulum kinase （PERK）. Ultrastructural changes of ER and lamellar bodies in AT2 cells were observed by transmission electron microscopy （TEM）. The expression levels of key proteins involved in ER stress and apoptosis pathways， including PERK， activating transcription factor 4 （ATF4）， and Caspase-3， were detected by Western blot. Double immunofluorescence staining of SPC and Ki-67 antigen （Ki-67） was performed to evaluate the proliferative capacity of AT2 cells. Lineage tracing technology （labeling AT2 cells with GFP） combined with Krt8 labeling was used to evaluate intermediate differentiation states， and morphological transformation of AT2 cells into alveolar type Ⅰ epithelial cells （AT1） was observed. ResultsBLM-induced mice exhibited significant structural disruption of lung tissue， increased collagen deposition， elevated lung coefficient， decreased pulmonary function， and upregulation of fibrosis-related factors （P<0.01）. High-dose N2FBR treatment significantly ameliorated lung tissue damage and dysfunction， significantly reduced HYP content （P<0.01）， and significantly downregulated ColIa1， α-SMA， and Timp1 expression （P<0.01）. Apoptosis analysis showed increased TUNEL-positive and Caspase-3-positive AT2 cells in the model group， which was significantly reduced by high-dose N2FBR treatment. TEM revealed swollen ER structures in AT2 cells of the model group， which tended to return to normal following treatment. PERK protein staining analysis showed evident ER stress in AT2 cells of the model group， which were markedly alleviated in the treatment group. The expression levels of ER stress-related proteins PERK and ATF4， as well as the apoptosis-related protein Caspase-3， were elevated in the model group and significantly reduced after treatment. TEM also revealed disrupted lamellar body structures in the model group， which tended to recover in the treatment group. Regarding the proliferative capacity of AT2 cells， the proportion of Ki-67⁺SPC⁺ AT2 cells significantly increased in the treatment group （P<0.01）. Lineage tracing showed that the proportion of keratin 8-positive green fluorescent protein-positive （Krt8⁺GFP⁺） cells increased in the model group， indicating differentiation arrest. This proportion was significantly reduced in the treatment group， and the morphology of GFP⁺ cells exhibited a flattened， extended shape， suggesting restored differentiation toward AT1 cells. ConclusionN2FBR alleviates ER stress in AT2 cells， reduces AT2 cell apoptosis， restores lamellar body structure and function， enhances proliferation activity， and alleviates differentiation arrest to promote differentiation into AT1 cells， thereby repairing the alveolar epithelium and effectively blocking the progression of pulmonary fibrosis. Its traditional Chinese medicine mechanism of "replenishing Zong Qi， harmonizing Qi and blood， and unblocking pulmonary meridians" closely aligns with the modern regulatory pathway of AT2 stem cells， providing a novel theoretical basis and experimental evidence for the intervention of IPF with traditional Chinese medicine.

An ideal dermal filler should integrate filling, repair, and anti-aging effects, with immediate tissue augmentation, slow degradation, and progressive stimulation of collagen regeneration. However, commonly used hyaluronic acid (HA) hydrogels, while effective for rapid filling, suffer from limited duration of support, weak cell adhesion, and an inability to promote collagen regeneration. Silk fibroin (SF), a natural protein from silkworm cocoons, is known for its excellent cell adhesion and collagen-stimulating abilities. However, its limited gelation capability restricts its potential application as a standalone injectable hydrogel. Based on a complementary strategy, this study combines the rapid gelling properties of HA with the collagen regenerative properties of SF to create a co-crosslinked HA-SF hydrogel. The composite hydrogel merges HA's rapid filling effect with SF's strong tissue adhesion and collagen-stimulating abilities. The formulation, physicochemical properties, degradation, biocompatibility, and filling effects of the HA-SF hydrogel were systematically investigated. HA-SF hydrogel exhibits excellent mechanical properties and ensures long-term support while maintaining injectability. Interestingly, after intradermal injection in the UVB-induced photoaging model, HA-SF hydrogel not only enhances hydrogel-cell interaction but also continues to stimulate collagen regeneration, especially type III collagen. This dual action achieves the biological effects of repair and anti-aging while maintaining the filling effect. Proteomic analysis confirms that repair and anti-aging effects are enhanced by the regulation of skin fibroblasts and modulation of amino acid and lipid metabolism. This composite hydrogel holds strong promise for clinical applications, offering a safer, long-lasting, and more natural injectable filler that combines filling, repair, and anti-aging into one system.

Objective To investigate the effect and underlying mechanism of bufalin regulating ferroptosis on extracellular matrix synthesis in renal tubular epithelial cells(RTECs)under high glucose(HG)conditions.Methods RTECs were cultured in vitro and exposed to HG.The experimental groups included:the control group,the HG group,the HG+dimethyl sulfoxide(DMSO)group,the HG+bufalin group,the HG+ferrostatin-1(Fer-1)group,the HG+bufalin+DMSO group and HG+bufalin+erastin group.The expression levels of fibronectin(FN),type Ⅰ collagen(Col Ⅰ),acyl-CoA synthetase long-chain family member 4(ACSL4),solute carrier family 7 member 11(SLC7A11)and glutathione peroxidase 4(GPX4)were detected using Western blot assay and quantitative real-time PCR(qRT-PCR).The potential molecular targets of bufalin were predicted using SwissTargetPrediction,and functional enrichment analysis was conducted using Metascape.FerrDb was employed to analyze ferroptosis-related gene sets.The levels of ferrous ions(Fe2+),malondialdehyde(MDA)and glutathione(GSH)were measured using micro-methods to evaluate the occurrence of ferroptosis.Results Compared with the control group,the mRNA and protein relative expression levels of FN,Col Ⅰand ACSL4 were increased in the HG group,while the mRNA and protein expression levels of GPX4 and SLC7A11 were decreased(P＜0.05).Compared with the HG+DMSO group,the mRNA and protein expression levels of FN,Col Ⅰand ACSL4,as well as levels of Fe2+and MDA were decreased in the HG+bufalin group,while the mRNA and protein expression levels of GPX4 and SLC7A11,and the level of GSH were increased(P＜0.05).In the HG+Fer-1 group,the mRNA and protein expression levels of GPX4 and SLC7A11 were increased,while the mRNA and protein expression levels of ACSL4,FN and Col Ⅰ were decreased(P＜0.05).The SwissTargetPrediction database and Metascape analysis function showed that the downstream functions of bufalin were closely related to lipid metabolism,inflammatory response,programmed cell death and ferroptosis-related pathways.The FerrDb analysis results indicated that the target sites of bufalin were closely related to ferroptosis markers.Compared with the HG+bufalin+DMSO group,the mRNA and protein expression levels of GPX4 and SLC7A11 were decreased in the HG+bufalin+Erastin group,while the mRNA and protein expression levels of ACSL4,FN and Col Ⅰ were increased(P＜0.05).Conclusion Bufalin attenuates extracellular matrix synthesis in HG-induced RTECs by inhibiting ferroptosis.

Sweat pore serves as the central regulator for ascending， descending， exiting and entering of qi movement， the circulation of essence， blood， and body fluids， and the nourishment of zang-fu organs. Its proper function depends on maintaining smooth flow and avoiding stagnation. Cough variant asthma （CVA）， in traditional Chinese medicine， falls under the "wind cough" category. The dysfunction of sweat pores' opening， closing， ascending， and descending is integral to the pathogenesis of CVA. This article focused on the dynamic changes in sweat pores' dysfunction throughout the progression of CVA， categorized into three stages，i.e. loss of pivot function， blockage of sweat pores， and lack of nourishment. The treatment approach centers on "wind medicinal opening sweat pores"， so for the initial stage， the focus is on activating sweat pores and dispelling wind， diffusing the lungs and rectifying qi； for the progression stage， the strategy shifts to unblocking sweat pores and dispersing wind， clearing lung stagnation and resolving obstructions； for the resolution stage， the emphasis is on nourishing sweat pores and defending against wind， strengthening the lungs and consolidating the body's foundation. This approach provides a systematic approach to the clinical diagnosis and treatment of CVA.

Objective:To investigate the role of dynamic changes in liver stiffness measurement (LSM) in predicting liver-related end-point events (LREs) occurrence in patients with chronic hepatitis B (CHB) with liver fibrosis during long-term antiviral therapy.Methods:Data were collected from CHB patients whose liver biopsy results showed Metavir fibrosis stage F2～F4 or clinically diagnosed cirrhosis. Entecavir antiviral therapy was mainly administered. Follow-up was conducted once every six months. Clinical data such as demographic information, blood routine tests, liver biochemical parameters, HBV virological and serological test results, and LSM were collected. Dynamic changes in LSM were categorized into four types based on LSM levels before treatment (0y) and following two years of antiviral therapy (2y) : (1) LSM 0y < 10 kPa and LSM 2y < 10 kPa, i.e., LSM persisted < 10 kPa; (2) LSM 0y < 10 kPa and LSM 2y ≥ 10 kPa, i.e., LSM increased to ≥ 10 kPa; (3) LSM 0y ≥ 10 kPa and LSM 2y < 10 kPa, i.e., LSM decreased to < 10 kPa; (4) LSM 0y ≥ 10 kPa and LSM 2y ≥ 10 kPa, i.e., LSM persisted ≥ 10 kPa. The predictive role of the dynamic changes of LSM in the occurrence of LREs was analyzed. The Wilcoxon rank-sum test was used for quantitative data. Fisher's exact test was used for categorical data. Multivariate analysis was performed using the Cox proportional hazards regression model. Survival curves were plotted and compared using the Kaplan-Meier. Results:A total of 713 CHB cases with liver fibrosis were included, among whom 512 had cirrhosis. The cumulative incidence of LREs following two years of antiviral therapy was low in patients with LSM 0y < 10 kPa during follow-up (all patients: LSM persisted < 10 kPa 1.6% vs. LSM increased to ≥ 10 kPa 0%; cirrhosis subgroup: LSM persisted < 10 kPa 0% vs. LSM increased to ≥ 10 kPa 0%). The 5-year cumulative incidence of LREs following two years of antiviral treatment was significantly higher in patients with LSM0y ≥ 10 kPa than in those with LSM persisting ≥ 10 kPa and those with LSM decreasing to < 10 kPa during follow-up (all patients: LSM persisted ≥ 10 kPa 12.4% vs. LSM decreased to < 10 kPa 3.6%; cirrhosis subgroup: LSM persisted ≥ 10 kPa 12.6% vs. LSM decreased to < 10 kPa 4.3%). Patients with LSM persisting at ≥ 10 kPa had a significantly increased risk of LREs following two years of antiviral treatment compared with those whose LSM decreased to <10 kPa during follow-up after adjusting for age, gender, baseline body mass index, platelet count, and alanine aminotransferase (all patients, aHR=2.96, 95% CI: 1.41～6.24, P=0.005; cirrhosis subgroup, aHR=2.74, 95% CI:1.26～5.95, P=0.011). Conclusions:LSM<10 kPa before antiviral treatment had a lower risk of liver-related endpoint events following two years of treatment among CHB patients with liver fibrosis. LSM ≥10 kPa before antiviral treatment and LSM persisted ≥10 kPa two years following treatment had a significantly higher occurrence risk of liver-related endpoints than LSM<10 kPa following treatment among CHB patients with liver fibrosis.

Objective To evaluate the quality of Xi xiong(Gansu Chuanxiong)based on the combination of intelligent sensory technology,HPLC and HS-SPME-GC-MS.Methods The chromaticity values of 10 batches of Gansu Chuanxiong Rhizoma samples were measured using a colorimeter and clustering analysis was performed;an electronic nose was used to measure the odor of Gansu Chuanxiong Rhizoma,and Loadings and PCA were conducted;According to the method under the Chuanxiaong Rhizoma section of the Chinese Pharmacopoeia,the moisture,ash content and extract were determined;HPLC was used to determine the contents of ferulic acid,chlorogenic acid and ligustrazine;the volatile components were analyzed by HS-SPME-GC-MS;the quality of Gansu Chuanxiong Rhizoma was evaluated by analyzing the correlation between chromaticity value,odor and active components.Results The total color value of Gansu Chuanxiong Rhizoma ranged from 31.210 1±1.193 7 to 43.976 3±0.721 4,at the Euclidean distance of 10,and the 10 batches of Gansu Chuanxiong Rhizoma could be clustered into four categories;Loadings and PCA showed that the higher contribution of sensors W2S,W5S,W2W,W1W and W1S to Gansu Chuanxiong Rhizoma samples,the variance contribution of the first and second principal components was 62.6%and 22.4%,respectively;water,ash and extract in 10 batches of Gansu Chuanxiong Rhizoma all met the standards of Chinese Pharmacopoeia;the HPLC determination results indicated that the content of ferulic acid in Gansu Chuanxiong Rhizoma was greater than 0.192 6%,ligustrazine content was between 0.001 2%and 0.006 1%,chlorogenic acid content was greater than 0.016 4%;HS-SPME-GC-MS results indicated 52 volatile components were identified in Gansu Chuanxiong Rhizoma samples,the olefin compounds were rich in species,phenyphthalide compounds had the highest relative content;the correlation analysis showed that the color values ΔL*,Δb* and ΔE showed a high degree of correlation with ferulic acid and ligusticum tecidate A.Conclusion This study clarifies the intrinsic quality of Gansu Chuanxiong Rhizoma and provides a theoretical basis for research on Gansu Chuanxiong Rhizoma.

[Objective]Based on the holistic view of"correspondence between nature and humans"in Huangdi Neijing,which is central to traditional Chinese time medicine theory,to explore a new diagnostic and therapeutic approach to insomnia from the perspective of"time".[Methods]By grounding in ancient and modern literature,this study elucidates the connotations of traditional Chinese time medicine and systematically reviews the temporal rhythms and derived theories related to insomnia in Huangdi Neijing,summarizing the approach to treating insomnia through time medicine.[Results]The disruption of the wake-sleep rhythm is a primary pathological mechanism of insomnia.The circadian rhythm,the four seasons rhythm,the exceeding the age rhythm and the meridians rhythm discussed in Huangdi Neijing are closely related to insomnia.They could be encapsulated into four major theories:the waxing and waning of Yin and Yang,the viscera and bowels managing time,the five movements and six climates,and the midnight-midday ebb flow theory.This study advocates a four-level strategy for insomnia,closely aligned with time medicine theory and the pathogenesis of insomnia,namely"regulating Yin and Yang""adapting to the four seasons""responding to annual Qi"and"reinforcement and elimination of Nazhi".[Conclusion]The time medicine concept in Huangdi Neijing has objectively effects in the prevention and treatment of insomnia,providing a new breakthrough and integration point for clinical diagnosis and treatment of insomnia.In clinical diagnosis and treatment of insomnia,the consideration of time rhythms should be fully integrated to achieve optimal therapeutic outcomes.

Objective To observe the mechanism of action of electroacupuncture at Neiguan(PC6)points for alleviating lipopolysaccharide(LPS)-induced myocadial dysfunction in sepsis model mice.Methods Forty-eight male C57BL/6 mice were randomly divided into four groups,namely normal control group,saline+electroacupuncture group,sepsis model group,and sepsis+electroacupuncture group.The rats in the sepsis model group and sepsis+electroacupuncture group were given intraperitoneal injection of LPS(5 mg/kg)to induce the sepsis model.The mice were treated with electroacupuncture immediately after injection.At hour 6 after the LPS intervention,the left ventricular short-axis end-systolic diameter(LVIDs)and fractional shortening(FS)of the left ventricular were monitored by color doppler echocardiography.The levels of inflammatory factors such as tumor necrosis factor alpha(TNF-α)and interleukin 6(IL-6)in serum were detected by enzyme-linked immunosorbent assay(ELISA),and the protein expression levels of Rho-kinase(ROCK)1 and ROCK2,and phosphorylation levels of myosin phosphatase substrate 1(MYPT1)and myosin light chain 2(MLC2)in cardiac tissues were detected by Western Blot.Results Compared with the normal control group,the LVIDs in mice in the sepsis model group was increased(P<0.05),FS was decreased(P<0.05),the levels of TNF-α and IL-6 in serum were all elevated(P<0.001),and the level of phosphorylation of MYPT1,a substrate of ROCK,in cardiac tissues was significantly elevated(P<0.05);compared with the sepsis model group,the LVIDs in the sepsis+electroacupuncture group was decreased(P<0.05),FS was increased(P<0.05),the levels of TNF-α and IL-6 in serum were decreased(P<0.05 or P<0.01),and the phosphorylation level of MYPT1 was significantly reduced(P<0.05),and the protein expression levels of ROCK1 and ROCK2 as well as the phosphorylation level of MLC2 had no significant differences(P>0.05).Conclusion Electroacupuncture at Neiguan points may reduce systemic and local inflammatory reaction levels in mice with sepsis model to improve cardiac function through inhibiting the activation of Rho/ROCK signaling pathway in cardiac tissues,thus producing myocardial protection efficacy.

Objective To explore the role of postdoctoral talent cultivation in high-quality development of public hospi-tals.Methods The data of 165 postdoctoral fellows were analyzed from Zhongshan Ophthalmology Center,Sun Yat-sen Univer-sity over the past decade.The analysis involved examining the entire management process from recruitment to completion,inclu-ding the improvement of relevant systems,evaluation standards,implementation of hierarchical management,mentor-student in-teractions,and academic exchanges,as well as studying the quality enhancement of the postdoctoral talent pool,research output,and employment analysis.Results The standardized management of whole postdoctoral cultivation process and the continuous improvement of systems significantly enhanced the achievements of postdoctoral fellows in research,publications,and commer-cialization of the scientific and research findings.For instance,from 2018 to 2022,the number of National Science Foundation-funded programs that the postdoctoral fellows obtained accounted for 26.7％of the total number,while the number of provincial and ministerial funded programs accounted for 73.3％.In 2020,the proportion of postdoctoral researchers who obtained the Na-tional Natural Science Foundation of China's Youth Program was 80％of the total.In 2021,the proportion of postdoctoral fellows who published papers with an impact factor of above 10 as the first author or co-first author was 45.83％.Conclusion The training of high-level medical postdoctoral talents is crucial for high-quality development of public hospitals,improving interdisci-plinary adaptability of postdoctoral fellows and collaborative mentorship awareness.