ObjectiveThis paper aims to observe the protective effect of Huamoyan granules on knee osteoarthritis （KOA） and explore whether its protective effect is oriented toward an anti-inflammatory direction by regulation of macrophage polarization， which can effectively inhibit the progression of pathological inflammatory response， reduce the release of inflammatory pain mediators， and downregulate the protein expression level of transient receptor potential vanilloid 1 （TRPV1）， so as to provide experimental evidence for its clinical application and investigate its action mechanism. MethodsAfter adaptive feeding， Sprague-Dawley （SD） rats were randomly divided into six groups： sham group， model group， celecoxib group， and high， medium， and low-dose synovitis granule groups （9.6， 4.8， 2.4 g·kg^-1）. The administration dose of celecoxib capsules was 20 mg·kg^-1. There were 10 rats in the sham group and 12 rats in the model group and each administration group. A KOA animal model was established by means of intra-articular injection of sodium iodoacetate into the knee joint. From the 10^th day of the experiment， each administration group was given intragastric administration at a dose of 10 mL·kg^-1 for 4 weeks. General conditions of rats in each group were assessed daily. The pressure pain threshold （PPT） to mechanical stimulation and joint diameter were recorded. X-ray examination was performed on the right knee joints of rats for imaging analysis. Enzyme linked immunosorbent assay （ELISA） was performed to detect the tumor necrosis factor-α （TNF-α）， serum interleukin-1β （IL-1β）， and other pro-inflammatory cytokines in rat serum samples， as well as the expression levels of neurogenic inflammatory mediators such as nerve growth factor （NGF） and calcitonin gene-related peptide （CGRP）. Histopathological changes in the knee joint synovial tissues were examined by hematoxylineosin （HE） staining. Safranin O-fast green staining was performed to observe and evaluate the degree of knee cartilage lesions. Western blot was employed to quantitatively analyze TRPV1， p38 mitogen-activated protein kinase （p38 MAPK）， and phosphorylated （p）-p38 MAPK in rat knee synovial tissues. Immunofluorescence （IF） was used to measure and assess M1/M2 macrophage polarization. ResultsCompared with those in the sham group， the circumference and joint diameter of the right knee were markedly enlarged in the model group （P<0.01）， while PPTs of rats showed a significant reduction （P<0.01）. The contents of IL-1β， TNF-α， CGRP， and NGF in rats' serum were significantly elevated （P<0.01）， and the synovial Krenn score was increased （P<0.01）. The Mankin score of cartilage tissue was increased （P<0.01）， and the protein expressions of TRPV1 and p-p38 MAPK/p38 MAPK were significantly upregulated （P<0.01）. The experimental intervention significantly reduced the proportion of pro-inflammatory M1 macrophages in the total macrophage population （P<0.01）， and the percentage of M2 macrophages was decreased （P<0.01）. The M1/M2 macrophage ratio was significantly elevated （P<0.01）. Knee joint diameters of all dose groups of Huamoyan granules and the celecoxib group were reduced （P<0.01） compared with those of the model group， and the PPT recovery speeds in the high and medium-dose groups of Huamoyan granules were more obvious （P<0.05）. The contents of IL-1β， CGRP， and NGF in the rats' serum in all administration groups were significantly reduced （P<0.05， P<0.01）， and the content of TNF-α in rats' serum was significantly reduced （P<0.01）. All dose groups of Huamoyan granules demonstrated significant reductions in both synovial Krenn score （P<0.05， P<0.01） and protein expression of TRPV1 and p-p38 MAPK/p38 MAPK in rats' synovial tissues （P<0.01）. The percentage of M1 macrophages in the synovial tissues of the celecoxib group and all dose groups of Huamoyan granules was decreased （P<0.01）. The percentage of M2 macrophages was increased （P<0.05）， and the M1/M2 ratio was decreased （P<0.01）. ConclusionHuamoyan granules can alleviate the inflammatory response of KOA， reduce the release of inflammatory pain mediators， and downregulate TRPV1 protein expression by regulating macrophage polarization. Its mechanism may be related to the TRPV1/p38 MAPK signaling pathway， thereby achieving the effect of improving peripheral pain hypersensitivity in KOA.

As a distinctive resource of Chinese civilization， traditional Chinese medicine （TCM） technology transfer faces significant opportunities under the background of digital and intelligent transformation， while also being constrained by unique challenges such as the complexity of its theoretical system， lengthy industrial chains， and multidimensional policy restrictions， resulting in a "high-value-high-threshold" paradox. At present， TCM technology transfer is deeply trapped in a "threefold reluctance" dilemma， i.e.， unwillingness to transfer， inability to transfer， and lack of capacity to transfer. Specifically， the disconnection between scientific research evaluation systems and market demand leads to low conversion rates of research achievements， unclear ownership and compliance risks suppress innovation incentives， and the absence of professional services intensifies supply-demand mismatches. This article systematically analyzes the specific characteristics of TCM technology transfer and proposes a breakthrough pathway centered on full-chain digital and intelligent transformation. By integrating technologies such as intelligent sorting systems， blockchain-based traceability， and AI diagnostic models， the TCM ecosystem spanning "cultivation-production-service" can be reconstructed. In terms of standardization， promoting the progression from "experience-based data conversion" to "data standardization" and further to "intelligent standardization" is advocated to resolve quality control challenges. For example， a "three-no-one-full" certification system can strengthen quality trust. Policy coordination should focus on optimizing mechanisms for the transformation of scientific and technological achievements， while exploring intellectual property securitization and risk-sharing models to stimulate research momentum. In terms of internationalization， reliance on the Belt and Road Initiative platform to promote the export of geo-authentic medicinal material brands and standards is recommended to build a dual-driven model of "technology plus culture". Looking ahead， through the construction of national-level databases， the cultivation of interdisciplinary talent， and the mutual recognition of international standards， a new paradigm of "scientific intelligent manufacturing" can be formed， providing systematic solutions for the modernization of TCM and global health governance.

Glaucoma and cataract are leading causes of blindness globally and frequently coexist in the elderly population, presenting unique challenges for clinical management. With continuous advancements in cataract surgery and the increasing diversity of intraocular lens(IOL)designs, optimizing IOL selection for patients with both glaucoma and cataract has emerged as a critical area of research. The goal is to achieve the best possible visual quality while maximizing the preservation of visual function, controlling intraocular pressure, and minimizing postoperative complications. This review systematically summarizes current research progress regarding IOL selection for patients with glaucoma and cataract.

Diabetic kidney disease（DKD） is a chronic kidney structural and functional disorder caused by diabetes. With the global prevalence of diabetes continuing to rise， DKD has gradually become a major cause of chronic kidney disease and end-stage renal disease（ESRD）， posing a serious threat to patients' quality of life and long-term health outcomes. Studies have shown that apoptosis plays a pivotal role in the development and progression of DKD， with its mechanisms involving abnormal activation of multiple signaling pathways such as Toll-like receptor 4（TLR4）/nuclear transcription factor-κB（NF-κB）/B-cell lymphoma-2（Bcl-2）/cysteinyl aspartate-specific proteinase（Caspase）-3， protein kinase R-like endoplasmic reticulum kinase（PERK）/eukaryotic initiation factor 2α（eIF2α）/activating transcript factor 4（ATF4）/CCAAT enhancer-binding protein homologous protein（CHOP）， phosphatidylinositol 3-kinase（PI3K）/protein kinase B（Akt）/glycogen synthase kinase-3β（GSK-3β）， Janus kinase 2（JAK2）/signal transducer and activator of transcription 3（STAT3）， adenosine monophosphate-activated protein kinase（AMPK）/mammalian target of rapamycin（mTOR） and silent information regulator 1（SIRT1）/tumor suppressor protein 53（p53）， thereby accelerating renal pathological damage in DKD. Extensive evidence-based medical studies have confirmed that traditional Chinese medicine（TCM）， leveraging its unique therapeutic advantages of multi-target， multi-component and multi-pathway approaches， has demonstrated remarkable efficacy and favorable safety profiles in treating DKD. Recent studies have demonstrated that active components of TCM can specifically target and modulate key effectors in apoptotic signaling pathways. Meanwhile， traditional compound formulations exert synergistic effects through multiple approaches such as replenishing deficiency and activating blood circulation， detoxifying and dredging collaterals， tonifying kidney essence， and removing stasis and purging turbidity， thereby comprehensively regulating critical pathological processes including endoplasmic reticulum stress and mitochondrial apoptosis pathways. This combined therapeutic approach of molecular targeting and holistic regulation provides novel strategies for delaying the progression of DKD. Based on this， this paper provides an in-depth analysis of key apoptotic signaling pathways and their regulatory mechanisms， while systematically summarizing recent research advances regarding the therapeutic effects of TCM active components， compound formulations， and proprietary Chinese medicines on DKD through modulation of these pathways， with particular emphasis on their underlying molecular mechanisms. These findings not only elucidate the modern scientific connotation and theoretical basis of TCM in treating DKD but also establish a solid theoretical and practical foundation for promoting the wider clinical application and further research of TCM in the field of DKD treatment.

Traditional treatment for type 1 diabetes mellitus （T1DM） primarily involves insulin replacement， yet some patients encounter issues such as significant blood glucose fluctuations， high risk of hypoglycemia， and weight gain. In recent years， the adjuvant therapeutic role of non-insulin hypoglycemic drugs in T1DM has gradually gained attention. This article reviews the mechanisms of action and clinical research progress of five types of non-insulin hypoglycemic drugs in the treatment of T1DM： amylin analogues （pramlintide）， biguanides （metformin）， sodium-glucose co-transporter 2 inhibitor， dipeptidyl peptidase-4 inhibitor， and glucagon-like peptide-1 receptor agonist. It is found that these drugs can enhance clinical benefits for T1DM patients by improving insulin sensitivity， delaying gastric emptying， promoting urinary glucose excretion， and regulating incretin levels， thereby reducing glycated hemoglobin levels， decreasing insulin dosage， and managing body weight. Simultaneously， these drugs also present limitations such as low patient compliance due to complex dosing regimens， increased risk of diabetic ketoacidosis， and heterogeneity in glycemic control. Future research could focus on developing individualized treatment strategies， combining pharmacogenomics with novel biomarkers to precisely identify subpopulations of patients who may benefit， and delving into the potential value of these drugs in delaying diabetic vascular complications and improving patients’ quality of life.

Objective:To investigate the correlation between serum calcium binding protein S100A9 levels and lung function in patients with idiopathic pulmonary fibrosis (IPF).Method:A retrospective case-control study was conducted. Forty patients diagnosed with IPF in respiratory department from January 4, 2023, to January 30, 2024 were selected as the IPF group,with a mean age of (65.3±8.4) years old, including 29 males and 11 females. while 50 healthy volunteers receiving health examinations in our physical examination center were enrolled in this study, including 38 males and 12 females, with a mean age of (64.1±6.3) years. The levels of biochemical parameters were assayed with biochemical analyzer. S100A9 levels were determined by Enzyme linked immunosorbent assay. The lung function test results of all participants were recorded. SPSS 19.0 statistical software was used to compare the differences of biomarkers levels between the two groups , Using parameter testing (independent sample t-test) to compare the differences in serum S100A9 levels and lung function between the two groups, the enumeration data were treated with the chi-square test. Pearson correlation analysis was used to evaluate the correlation between S100A9 and lung function, the influencing factors of IPF were analyzed by using multivariate logistic regression model, and receiver operating characteristic (ROC) curve analysis was used to assess the value of Calprotectin S100A9 in predicting IPF. Results:The serum S100A9 levels in the IPF group were significantly higher than those in the healthy control group [(132.47±21.46) pg/ml,(44.75±8.84) pg/ml, t=3.544, P<0.05], forced expiratory volume in one second(FEV1,1.38±0.19) L, forced vital capacity (FVC, 2.38±0.59) L, FEV1/FVC (57.98±6.13), the maximum spontaneous ventilation (MVV, 57.48±7.66) L/min was lower than that of the control group [(3.24±0.65) L, (3.65±0.67) L, (88.77±7.97), (86.34±7.23) L/min, t=3.486,3.393,2.771,3.462, P<0.05]. Serum S100A9 was negatively correlated with FEV1, FVC, FEV1/FVC, and MVV ( r=-0.537,-0.458,-0.489,-0.511, P<0.05), S100A9 was positively correlated with S100A9 in bronchoalveolar lavage fluid and high-resolution CT fibrosis score ( r=0.632, r=0.517, P<0.05).The area under the curve (AUC) of S100A9 for predicting IPF was 0.691. Conclusion:The level of calcium binding protein S100A9 was significantly increased in IPF patients, and was closely related to decreased lung ventilation function and the occurrence of IPF, which might serve as a marker for evaluating pulmonary fibrosis.

Cell death is a fundamental phenomenon for organisms to maintain their basic morphology.When a pathogen infects a cell,the process of programmed cell death is activated,the lysed cells carrying the pathogen ac-tivate the immune response of the organism in the process of removing infected cells,thus exerting immune de-fense.The molecular mechanisms of the 4 types of cell death modes apoptosis,pyroptosis,necroptosis and pan-apoptosis as well as their effects on innate immune defense against microbial infections were mainly elaborated in the article,the interactions among the different programmed cell death pathways were briefly interpreted so as to provide new ideas for further study of pathogenic mechanisms of infectious diseases.

Objective:As a crucial support for high-level innovation and high-efficiency transformation in research-oriented hospitals, the construction and operation mechanisms of scientific and technological innovation platforms need to be rationalized to ensure their efficient operation. This is a key issue that research-oriented hospitals should focus on and resolve in the process of scientific and technological management.Methods:Xiangya Hospital of Central South University had seized the construction of scientific and technological innovation platforms as a handle. It innovated management methods in key links such as platform cultivation and layout, investment of scientific and technological resources, paid use of space, performance assessment of platforms, and sharing of scientific research equipment. By doing so, it optimized the allocation of resources, stimulated innovative vitality, and created a new ecosystem for the innovative development of the hospital.Results:The efficient and coordinated development of the hospital′s scientific and technological innovation platforms had significantly enhanced the hospital′s overall capacity for scientific and technological innovation.Conclusions:Strengthening the construction of scientific and technological innovation platforms in research-oriented hospitals can effectively enhance the overall scientific and technological innovation strength and level of research-oriented hospitals, which can provide reference and reflection for domestic research-oriented hospitals to accelerate the achievement of high-level innovation and high-quality development goals.

A 62-year-old male, was admitted to the hospital, with a chief complaint of fever lasting over 10 days and leukopenia and thrombocytopenia for 2 days. Ten days prior to admission, the patient experienced intermittent fever without obvious incentive factors. The breath sounds in both lungs were coarse, without accompanying dry or moist rales. Color Doppler Ultrasound indicated mild splenomegaly and multiple lymphadenectasis in the bilateral cervical, axillary, and inguinal regions. Morphological examination of bone marrow cells demonstrated abnormally large blasts, with some of the nuclei being rather irregular and cytoplasmic vacuoles. Immunophenotyping results identified this group of blast cells as immature monocytes. Karyotype analysis of chromosomes showed clonal abnormalities, with 19 out of 20 cells exhibiting near-tetraploid karyotypes, including complex karyotypic abnormalities involving chromosome17.Targeted next-generation sequencing (NGS) detected gene mutations associated with hematological malignancies that have definite or potential clinical significance,including TP53, SRSF2, STAG2, and ARID2, with variant allele frequencies (VAF) of 63.10%, 30.30%, 0.80%, and 0.60%, respectively. Integrating laboratory findings, the diagnosis was diagnosed as AML-M5 at high-risk. After receiving chemotherapy with the regimen of azacitidine combined with venetoclax, the patient passed away more than 20 days later.

AIM To investigate the effects of Changpu Yujin Decoction(CPYJD)on striatal mitophagy and PINK1/Parkin signaling pathway in a rat model of Tourette syndrome(TS).METHODS Thirty-six SPF male SD rats were randomly assigned to the control group(n=9)and the TS modeling group(n=27).Rats in the modeling group received daily intraperitoneal injections of 3,3'-iminodipropionitrile(IDPN)(300 mg/kg)for 7 consecutive days to establish the TS model.Post-modeling,successfully induced TS rats were re-randomized into model group(no treatment),tiapride group(47.91 mg/kg)and CPYJD group(77.28 g/kg).All groups received their respective interventions via intragastric administration daily for 28 days.Following drug administration,behavioral scores were assessed in each group.Pathological alterations in the striatum were examined using HE staining,while ultrastructural changes were evaluated by transmission electron microscopy(TEM).Neuronal apoptosis was quantified via TUNEL staining,and ROS levels in striatum were measured by ELISA.Co-localization of PINK1 and LC3B was assessed using immunofluorescence(IF).Finally,mRNA and protein expressions of PINK1,Parkin,Beclin-1,P62 and LC3B(LC3B-Ⅱ/Ⅰ ratio)were analyzed by RT-qPCR and Western blot.RESULTS Compared to the control group,the model group demonstrated significantly increased behavioral scores(P＜0.01),elevated neuronal apoptosis rate and higher ROS levels in the striatum(P＜0.01);severe neuronal and mitochondrial damage in the striatum;significantly reduced mRNA and protein expressions of PINK1,Parkin,Beclin-1 and LC3B(LC3B-Ⅱ/Ⅰ ratio)in the striatum(P＜0.01);markedly upregulated P62 mRNA and protein expressions(P＜0.01).Compared to the model group,both the tiapride and CPYJD intervention groups exhibited significantly reduced behavioral scores(P＜0.01);decreased neuronal apoptosis rate and lower ROS levels(P＜0.01);improved pathological alterations in the striatal neurons and mitochondria;increased mRNA and protein expressions of PINK1,Parkin and Beclin-1 in the striatum(P＜0.05,P＜0.01);and decreased P62 mRNA and protein expressions(P＜0.01).Furthermore,the rats in the CPYJD group specifically showed elevated LC3B mRNA level and LC3B-Ⅱ/Ⅰ protein ratio in striatum(P＜0.05,P＜0.01).CONCLUSION The effect of CPYJD intervention in TS rats may involve activation of mitophagy through regulation of the PINK1/Parkin signaling pathway,improving mitochondrial function,reducing ROS levels,and thereby protecting neurons.