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.

OBJECTIVE To clarify the roles and functions of full-time pharmacists in the management of early-phase clinical trials of antineoplastic drugs， and to provide theoretical and practical support for their transformation from traditional drug managers to multi-dimensional roles in clinical research. METHODS Combined with relevant regulations such as the Good Clinical Practice （GCP） （2020 Edition）， and based on the clinical practice experience of the Phase Ⅰ Clinical Ward in our hospital， this study systematically sorted out full-time pharmacists’ roles and functions in early-phase clinical trials of antineoplastic drugs， and explored the core challenges and optimization pathways for role transformation and capacity-building of domestic full-time clinical trial pharmacists. RESULTS & CONCLUSIONS Full-time pharmacists assumed multiple roles in early-phase clinical trials of antineoplastic drugs， including providing pharmaceutical support for protocol design， implementing whole-process standardized management of clinical trial drugs， ensuring medication safety for clinical trial subjects/participants， conducting quality control throughout the clinical trial process， and serving as a bridge for interdisciplinary collaboration and communication. Currently， there are challenges in this field in China， such as unclear roles， an imperfect capacity building system， and insufficient regulatory support. This paper proposes that by establishing a standardized role framework， clarifying the core responsibilities and authorities of full-time pharmacists， and leveraging cutting-edge technologies to provide comprehensive support for their roles， so as to fully harness their pharmaceutical expertise and contribute to the standardization and efficiency of the antineoplastic new drug development process.

Objective: To establish an accurate and rapid typing method for Rh typing of samples from patients who have received recent blood transfusions by utilizing the difference in osmotic fragility between fresh and old red blood cells. Methods: A lysing solution suitable for destroying old RBCs was prepared. Sixty-one samples collected in our hospital in 2024 with Rh typing of double groups were treated with the lysing solution to remove the old allogeneic red blood cells while preserving the patient's own fresh red blood cells, followed by repeat Rh typing tests. Results: For 61 samples with Rh typing in double groups, 41 were accurately detected identified through the red blood cell lysis method, yielding an identification rate of 67.21%. No significant difference was observed compared to the detection rate of the commonly used capillary centrifugation modified method (χ =0.103, P>0.05). Conclusion: The red blood cell lysis method provides a novel and rapid experimental approach for clinical use in processing Rh-typed samples that are of double groups, thereby offering a basis for Rh compatibility blood transfusion.

Objective: To explore the application effectiveness of healthcare failure mode and effect analysis (HFMEA) in optimizing intelligent blood logistics transport pathways for safety assurance. Methods: Data from 1 851 cases of intelligent blood logistics transport were collected between September 2023 and March 2025. Based on the implementation phases of HFMEA measures, the cases were divided into a control group (n=120), observation group 1 (n=219), and observation group 2 (n=1 512). Through systematic analysis of the transport processes, hazard scoring and decision tree analysis were conducted for each process, and phased optimization measures were implemented for high-risk failure modes. Results: The transport duration of intelligent blood logistics was 35.5 (20.8, 71.1) min in the control group, 25.1 (10.9, 40.7) min in observation group 1, and 9.9 (4.2, 44.5) min in observation group 2. Observation group 2 exhibited significantly shorter transport time compared to both observation group 1 and the control group, with statistically significant differences between groups (P<0.000 1). Conclusion: The implementation of HFMEA-driven measures significantly reduced intelligent blood logistics transport duration, thereby fostering the evolution of smart hospital ecosystems while enhancing healthcare service quality and operational efficiency.

Objective To investigate the effect of bone metabolic markers on sarcopenia in elderly patients with type 2 diabetes mellitus (T2DM). Methods A total of 412 patients with T2DM in the department of endocrinology of Nanjing Central Hospital from May 2020 to June 2025 were selected as the research subjects. According to Asian Working Group for Sarcopenia (AWGS) in 2019, these patients were evaluated for skeletal muscle mass index (ASMI), muscle strength, and muscle function, and were divided into a sarcopenia group (84 cases) and a non-sarcopenia group (328 cases). The glucolipid metabolic indexes were detected in both groups of patients, and the bone metabolic markers were evaluated, including procollagen type 1 N-terminal peptide (P1NP), beta-C-terminal telopeptide of type 1 collagen (β-CTX), and 25-hydroxy vitamin D [25-(OH)D]. The factors influencing the occurrence of sarcopenia in T2DM patients were analyzed by logistic regression analysis, and the diagnostic values of bone metabolic markers on sarcopenia in patients with T2DM were assessed by ROC curve. Results The levels of P1NP and 25-(OH)D were lower, while β-CTX level was higher in the sarcopenia group compared to the non-sarcopenia group, with statistical differences (P<0.05). After logistic correlation analysis, it was found that P1NP, β-CTX and 25-(OH)D were all influencing factors for the occurrence of sarcopenia in T2DM patients. ROC curve analysis suggested that combined detection of PINP, β-CTX, and 25-(OH)D had higher diagnostic value, with an area under the curve up to 0.805. Conclusion The abnormal expression of bone metabolic markers is associated with the increased risk of sarcopenia in patients with T2DM. The detection of serum bone metabolic markers expression level is of certain significance for the assessment of diabetes-related sarcopenia.

ObjectiveTo investigate the mechanism by which adrenoceptor alpha 2A (Adra2a) regulates lipopolysaccharide (LPS)-induced inflammation in primary hepatocytes from lipopolysaccharide-binding protein (LBP) knockout mice (Lbp^-/-). MethodsPrimary hepatocytes from C57BL/6J and Lbp^-/- mice were isolated using a two-step perfusion method. An in vitro inflammatory model was established by LPS stimulation, and an in vivo inflammatory mouse model was established by intraperitoneal injection of LPS. The in vitro experiments were grouped as follows: Control group, LPS group, BRL+LPS group, OE-NC+LPS group, and OE-Adra2a+LPS group. The Control group served as the blank control. The LPS group involved stimulating primary hepatocytes with LPS. The BRL+LPS group involved pretreating primary hepatocytes with BRL-44408 maleate followed by LPS stimulation. The OE-NC+LPS group involved transfecting primary hepatocytes with an empty vector followed by LPS stimulation. The OE-Adra2a+LPS group involved transfecting primary hepatocytes with a lentivirus overexpressing Adra2a, followed by LPS stimulation. The in vivo experimental groups were divided into Control', LPS', BRL+LPS', OE-NC+LPS', and OE-Adra2a+LPS' groups. The Control' group served as the blank control. The LPS' group received intraperitoneal injection of LPS. The BRL+LPS' group received intraperitoneal injection of BRL-44408 maleate for pretreatment, followed by LPS injection. The OE-NC+LPS' group received intraperitoneal injection of empty vector for pretreatment, followed by LPS injection. The OE-Adra2a+LPS' group received intraperitoneal injection of a lentivirus overexpressing Adra2a for pretreatment, followed by LPS injection. Cell viability after Adra2a inhibition and overexpression was assessed via the Cell Counting Kit-8 (CCK-8) assay. RT-qPCR measured changes in gene expression levels of tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6), and interleukin-1β (IL-1β) after Adra2a inhibition and overexpression. Western blotting was performed to detect Adra2a protein expression and phosphorylation levels of extracellular signal-regulated kinase 1/2 (ERK1/2), p38 mitogen-activated protein kinase, and c-Jun N-terminal kinase (JNK) following LPS stimulation. ResultsIn vitro experiments revealed that LPS stimulation significantly decreased Adra2a protein expression in primary hepatocytes from C57BL/6J mice compared to the Control group (P<0.05), whereas it increased in primary hepatocytes from Lbp^-/- mice (P<0.001). Compared to the LPS group, the BRL+LPS group exhibited significantly increased cell viability (P<0.01), reduced TNF-α, IL-6, and IL-1β gene transcription levels (P<0.01, P<0.001, P<0.001), and decreased phosphorylation levels of MAPK signaling pathway-related proteins ERK1/2, p38, and JNK (P<0.01, P<0.001, P<0.001). Compared with the OE-NC+LPS group, the OE-Adra2a+LPS group showed significantly decreased cell viability (P<0.001), increased gene transcription levels of TNF-α, IL-6, and IL-1β genes (P<0.001, P<0.01, P<0.001), and elevated phosphorylation levels of MAPK signaling pathway-related proteins ERK1/2, p38, and JNK (P<0.001, P<0.01, P<0.001). In vivo experiments showed that, compared with the LPS' group, the BRL+LPS' group exhibited significantly reduced phosphorylation levels of MAPK signaling pathway-related proteins ERK1/2, p38, and JNK (P<0.001, P<0.01, P<0.01). In the OE-Adra2a+LPS' group, the phosphorylation levels of ERK1/2, p38, and JNK were significantly elevated compared to the OE-NC+LPS' group (P<0.01, P<0.001, P<0.01). ConclusionLPS stimulation can cause a significant increase in Adra2a protein expression in primary hepatocytes of Lbp^-/- mice. Adra2a protein can regulate the level of LPS-induced inflammation in primary hepatocytes of Lbp^-/- mice through the MAPK signaling pathway.

ObjectiveBased on 16S rDNA technology and molecular biology methods， the molecular mechanism of Shenling Baizhusan in the treatment of diarrhea-predominant irritable bowel syndrome （IBS-D） was investigated. MethodsThe 42 SD rats with SPF were randomly divided into no control group， SLBZS-H， medium （SLBZS-M）， low （SLBZS-L） dose group， positive control group and model group， with 7 rats in each group. The rat model of IBS-D was prepared by ice-cold senna （0.45 g∙mL^-1） gavage （10 mL∙kg^-1） combined with restraint stress for 14 consecutive days. After successful modeling， the corresponding drugs were given to each group with a gavage volume of 10 mL∙kg^-1： The positive group was administered with 2.36 ， 1.18， 0.59 g∙mL^-1 of Shenling Baizhusan in the Positive group and the Model group with the same volume of normal saline for 14 d. The general condition of the rats： Weight， feces， mental state and death were observed and recorded. The body weight， abdominal wall retraction reflex score （AWR） and loose stool rate of rats in each group were measured before （the first day）， after the model （day 14） and after treatment （day 28）. Hematoxylin-eosin staining was used to observe the morphological characteristics of colon tissues of experimental animals. Enzyme-linked immunosorbent assay was used to quantitatively analyze the concentration of inflammatory mediators in the peripheral blood of experimental animals. Western blotting was used to detect the expression levels of key proteins of Toll-like receptor 4 （TLR4）， Toll-like receptor 2 （TLR2）， myeloid differentiation factor 88 （MyD88） and nuclear factor-κB （NF-κB） signaling pathway in rat colon tissue. 16S rDNA technology was used to detect the structural changes of intestinal microbiota in rats. ResultsCompared with Control， the colon of the Model group showed partial mucosal epithelial shedding and inflammatory cell infiltration. The contents of TNF-α， IL-1β， IL-6 and 5-HT in serum increased （P<0.05）， the protein expressions of TLR2， TLR4， MyD88 and NF-κB in colon tissue increased （P<0.05）， the diversity indices of Richness， Chao1， abundance-based coverage estimator（ACE） and Shannon decreased （P<0.05）， and the phylum Firmicutes， Actinobacteria， The relative richness of Bacteroides-H， Lactobacillus and Ligilactobacillus decreased （P<0.05）， while the relative richness of Bacteroidetes， Proteobacteria and Prevotella increased （P<0.05）. Compared with the model group， the colonic structure and organization of the SLBZS-H group， SLBZS-M group， SLBZS-L group and Positive group were clearer， and only a small number of inflammatory cells were present in some areas， and the serum contents of TNF-α， IL-1β， IL-6 and 5-HT were decreased （P<0.05）， TLR2， TLR4， The protein expressions of MyD88 and NF-κB decreased （P<0.05）， and compared with the model group， the diversity indices of Richness， Chao1， ACE and Shannon in the SLBZS-H， SLBZS-M and SLBZS-L groups increased （P<0.05）， and the richness of Firmicutes and Actinobacteria increased （P<0.05）. The richness of Proteobacteria and Prevotella decreased （P<0.05）， and the abundance of Prevotella decreased （P<0.05）， Bacteroides-H， Muribaculum， Lactobacillus and salivarius in the Positive group salivarius （P<0.05）. ConclusionShenling Baizhusan can effectively treat IBS-D， and its molecular mechanism may be to play a therapeutic role by improving intestinal flora and inhibiting the TLRS/MyD88/NF-κB signaling pathway to reduce inflammatory response.

ObjectiveThis study aimed to investigate whether Bushen Tongluo prescription inhibits macrophage polarization by regulating the Wnt3a/β-catenin signaling pathway， thereby reducing epithelial-mesenchymal transition and excessive extracellular matrix deposition， in order to elucidate the anti-pulmonary fibrosis mechanisms of Bushen Tongluo prescription and provide a new theoretical basis for the clinical treatment of pulmonary fibrosis. MethodsFifty male Sprague-Dawley （SD） rats were randomly divided into a blank group， model group， pirfenidone group， and high- and low-dose Bushen Tongluo prescription groups. Except for the blank group， the pulmonary fibrosis model was established by intratracheal instillation of bleomycin. Intervention was initiated on day 28 after modeling. The high- and low-dose Bushen Tongluo prescription groups were administered Bushen Tongluo prescription at doses of 30.88， 15.44 g·kg^-1， respectively， by intragastric gavage. The pirfenidone group was administered pirfenidone capsules at 110 mg·kg^-1 by intragastric gavage. The blank and model groups were given an equal volume of normal saline by gavage， once daily for 90 days. After treatment， the level of transforming growth factor-β₁ （TGF-β₁） in bronchoalveolar lavage fluid （BALF） was detected by enzyme-linked immunosorbent assay （ELISA）. Morphological changes in lung tissue and the collagen volume fraction were compared. The protein distribution and expression of E-cadherin， cytokeratin 19， α-smooth muscle actin （α-SMA）， vimentin， collagen type Ⅰ （Col Ⅰ）， and collagen type Ⅲ （Col Ⅲ） in lung tissue were detected by immunohistochemistry. The protein distribution and expression of CD68， arginase-1 （Arg-1）， inducible nitric oxide synthase （iNOS）， Wnt3a， and β-catenin in lung tissue were detected by immunofluorescence. The protein expression of Wnt3a and β-catenin in lung tissue was detected by Western blot， and the mRNA expression of Wnt3a and β-catenin was detected by Real-time fluorescence quantitative polymerase chain reaction （Real-time PCR）. ResultsCompared with the blank group， a large number of inflammatory cells infiltrated the airway walls， alveolar spaces， and interstitial tissue in the model group， with obvious fibrous tissue hyperplasia. The level of TGF-β₁ in BALF was significantly increased. The protein expression of E-cadherin and cytokeratin 19 in lung tissue was decreased， whereas the protein expression of α-SMA， Vimentin， Wnt3a， β-catenin， Col Ⅰ， and Col Ⅲ was increased. The fluorescence-positive area ratios of CD68， Arg-1， iNOS， Wnt3a， and β-catenin in lung tissue were increased. The protein and mRNA expression levels of Wnt3a and β-catenin in lung tissue were significantly increased （P<0.01）. Compared with the model group， all treatment groups showed varying degrees of improvement in inflammatory cell infiltration and fibrous tissue hyperplasia in the airway walls， alveolar spaces， and interstitial tissue， decreased TGF-β₁ levels in BALF， increased protein expression of E-cadherin and cytokeratin 19 in lung tissue， decreased protein expression of α-SMA， Vimentin， Col Ⅰ， and Col Ⅲ， decreased fluorescence-positive area ratios of CD68， Arg-1， iNOS， Wnt3a， and β-catenin in lung tissue， and decreased protein and mRNA expression levels of Wnt3a and β-catenin in lung tissue （P<0.05， P<0.01）. ConclusionBushen Tongluo prescription can improve bleomycin-induced pulmonary fibrosis in rats by inhibiting epithelial-mesenchymal transition and reducing excessive extracellular matrix deposition. The mechanism may be related to inhibition of the Wnt3a/β-catenin signaling pathway and the macrophage polarization mediated by this pathway.

Immune-stimulating antibody drug conjugate (ISAC) can not only effectively solve the defects of stimulator of interferon genes (STING) agonists by coupling antibodies with STING agonists through the targeting of antibodies, but also play a synergistic role with antibodies to further improve the efficacy of STING agonists. This review first provides a concise overview of the current research landscape of ISACs and STING agonists, systematically elaborates on evolving trends in STING agonist development, and subsequently summarizes the mechanistic advances in STING ISAC research. Special emphasis is placed on representative STING ISAC candidates in preclinical/clinical development. Finally, the future directions of STING ISACs are critically discussed with perspectives and recommendations, aiming to provide theoretical insights and practical guidance for future investigations.

Objective: To explore the nonlinear dynamic effects of social capital, adverse childhood experiences (ACEs) and depressive symptoms on suicidal behavior among vocational high school students, so as to provide theoretical basis and practical references for formulating suicide prevention strategies. Methods: A convenience sampling method was employed to include 668 students from a vocational high school from Wuhan in March 2023. Social capital was used as the asymmetry variable, while ACEs and depressive symptoms were used as bifurcation variables, a cusp catastrophe model was constructed to analyze the nonlinear changes in suicidal behavior among vocational high school students, and its fit was compared with linear and Logistic regression models. Results: Among students in the health vocational high school in Wuhan, only suicidal ideation accounted for 8.5%, only suicide attempt for 18.6%, neither accounted for 31.9%, and both for 41.0%. Gender, left behind experience, family economic status, parental parenting styles, depressive symptoms, social capital, and ACEs were all related factors influencing suicidal behavior among vocational high school students ( χ 2/H=19.03, 13.33, 21.11, 46.70, 144.38, 24.61, 118.77, all P <0.05). Violin plots showed a bimodal distribution of suicidal behavior, indicating nonlinear variation characteristics. The cusp catastrophe model results showed that social capital was negatively correlated with suicidal behavior, but the relationship was bifurcated by ACEs ( α social capital = -0.006 , β ACEs =0.075) and depressive symptoms ( α social capital =-0.013, β depressive =0.028) (all P <0.05). When both ACEs and depressive symptoms coexisted, the impact of ACEs was stronger ( β ACEs =0.077, β depressive =0.014) (both P <0.05). The cusp catastrophe model fitted ( R 2=0.886, 0.881, 0.882) better than the linear ( R 2=0.258, 0.219, 0.258) and Logistic regression models ( R 2= 0.242, 0.211 , 0.176). Gender stratified analysis results showed that bifurcation effect of ACEs was stronger in males than in females( β boys =0.224, β girls =0.086); in females, both ACEs and depressive symptoms had a bifurcation effect, with the former showing a stronger effect ( β ACEs =0.062, β depressive =0.015) (all P <0.05). Conclusions Suicidal behavior among vocational high school students exhibits nonlinear characteristics. Improving social capital to reducing ACEs and depressive symptoms may contribute to decreasing adolescent suicidal behaviors.