To explore the advantages of traditional Chinese medicine （TCM） and integrative TCM-Western medicine approaches in the treatment of diabetic microvascular complications （DMC）， refine key pathophysiological insights and treatment principles， and promote academic innovation and strategic research planning in the prevention and treatment of DMC. The 38th session of the Expert Salon on Diseases Responding Specifically to Traditional Chinese Medicine， hosted by the China Association of Chinese Medicine， was held in Beijing， 2024. Experts in TCM， Western medicine， and interdisciplinary fields convened to conduct a systematic discussion on the pathogenesis， diagnostic and treatment challenges， and mechanism research related to DMC， ultimately forming a consensus on key directions. Four major research recommendations were proposed. The first is addressing clinical bottlenecks in the prevention and control of DMC by optimizing TCM-based evidence evaluation systems. The second is refining TCM core pathogenesis across DMC stages and establishing corresponding "disease-pattern-time" framework. The third is innovating mechanism research strategies to facilitate a shift from holistic regulation to targeted intervention in TCM. The fourth is advancing interdisciplinary collaboration to enhance the role of TCM in new drug development， research prioritization， and guideline formulation. TCM and integrative approaches offer distinct advantages in managing DMC. With a focus on the diseases responding specifically to TCM， strengthening evidence-based support and mechanism interpretation and promoting the integration of clinical care and research innovation will provide strong momentum for the modernization of TCM and the advancement of national health strategies.

ObjectiveTo investigate the effects of Maxing Kugan decoction （MKD） on inflammatory response and apoptosis in rats with oleic acid （OA）-induced acute lung injury （ALI） and explore its mechanism of action. MethodsSixty Sprague-Dawley （SD） rats were randomly assigned into six groups： a control group， a model group， a dexamethasone-treated group （2 mg·kg^-1）， and three MKD-treated groups at low， medium， and high doses （3.1， 6.2，12.4 g·kg^-1）. Each group was administered either an equivalent volume of normal saline or the corresponding concentration of MKD by gavage for seven consecutive days. The model group and each administration group were used to establish the ALI model by tail vein injection of OA （0.2 mL·kg^-1）. Twelve hours after modeling， blood gas analyses were conducted， and the wet-to-dry （W/D） weight ratio of lung tissue was measured for each group. Additionally， enzyme-linked immunosorbent assay （ELISA） was employed to quantify the levels of tumor necrosis factor-alpha （TNF-α）， interleukin-1β （IL-1β）， and interleukin-6 （IL-6） in the bronchoalveolar lavage fluid （BALF） of the rats. Cell damage and apoptosis in lung tissue were examined via hematoxylin-eosin （HE） staining and TdT-mediated dUTP-biotin nick end labeling （TUNEL） assays， and the results were subsequently scored. The expression levels of the p38 mitogen-activated protein kinase （p38 MAPK）/nuclear factor kappa-B （NF-κB） signaling pathway and apoptosis-related proteins and mRNAs were assessed using Western blot and real-time fluorescence quantitative polymerase chain reaction （Real-time PCR）. ResultsCompared with the control group， the model group exhibited a significant decrease in partial pressure of oxygen （PaO₂）， blood oxygen saturation （SaO₂）， and oxygenation index （PaO₂/FiO₂）， along with a marked increase in partial pressure of carbon dioxide （PaCO₂） and lung W/D ratio （P<0.01）. Additionally， levels of TNF-α， IL-6， and IL-1β in BALF were significantly elevated （P<0.01）. Histopathological analysis of lung tissue showed significant inflammatory infiltration， tissue edema， alveolar septal thickening， and apoptosis of lung tissue. Pronounced increases were observed in the mRNA expression levels of p38 MAPK， NF-κB p65， inhibitor of NF-κB （IκBα）， B-cell lymphoma-2 associated x protein （Bax）， and Caspases-3， as well as the protein expression levels of p-p38 MAPK， p-NF-κB p65， p-IκBα， Bax， Caspases-3， and cleaved Caspases-3， while the mRNA and protein expression of Bcl-2 was downregulated （P<0.01）. Compared with the model group， MKD significantly elevated PaO₂， SaO₂， and PaO₂/FiO₂ while reducing PaCO₂ and W/D ratio in rats （P<0.01）. It also greatly reduced TNF-α， IL-6， and IL-1β levels in BALF （P<0.01） and alleviated inflammatory infiltration， tissue edema， alveolar septal thickening， and apoptosis of lung tissue. Additionally， it downregulated the mRNA expression of p38 MAPK， NF-κB p65， IκBα， Bax， Caspases-3， as well as protein expression of p-p38 MAPK， p-NF-κB p65， p-IκBα， Bax， Caspases-3， and cleaved Caspases-3 in lung tissue （P<0.05， P<0.01）， while significantly upregulating mRNA and protein expression of Bcl-2 （P<0.01）. ConclusionMKD exerts a protective effect on OA-induced ALI rats， potentially through the regulation of the p38 MAPK/NF-κB signaling pathway to inhibit inflammation and apoptosis.

ObjectiveTo investigate the effects of Maxing Kugan decoction （MKD） on inflammatory response and apoptosis in rats with oleic acid （OA）-induced acute lung injury （ALI） and explore its mechanism of action. MethodsSixty Sprague-Dawley （SD） rats were randomly assigned into six groups： a control group， a model group， a dexamethasone-treated group （2 mg·kg^-1）， and three MKD-treated groups at low， medium， and high doses （3.1， 6.2，12.4 g·kg^-1）. Each group was administered either an equivalent volume of normal saline or the corresponding concentration of MKD by gavage for seven consecutive days. The model group and each administration group were used to establish the ALI model by tail vein injection of OA （0.2 mL·kg^-1）. Twelve hours after modeling， blood gas analyses were conducted， and the wet-to-dry （W/D） weight ratio of lung tissue was measured for each group. Additionally， enzyme-linked immunosorbent assay （ELISA） was employed to quantify the levels of tumor necrosis factor-alpha （TNF-α）， interleukin-1β （IL-1β）， and interleukin-6 （IL-6） in the bronchoalveolar lavage fluid （BALF） of the rats. Cell damage and apoptosis in lung tissue were examined via hematoxylin-eosin （HE） staining and TdT-mediated dUTP-biotin nick end labeling （TUNEL） assays， and the results were subsequently scored. The expression levels of the p38 mitogen-activated protein kinase （p38 MAPK）/nuclear factor kappa-B （NF-κB） signaling pathway and apoptosis-related proteins and mRNAs were assessed using Western blot and real-time fluorescence quantitative polymerase chain reaction （Real-time PCR）. ResultsCompared with the control group， the model group exhibited a significant decrease in partial pressure of oxygen （PaO₂）， blood oxygen saturation （SaO₂）， and oxygenation index （PaO₂/FiO₂）， along with a marked increase in partial pressure of carbon dioxide （PaCO₂） and lung W/D ratio （P<0.01）. Additionally， levels of TNF-α， IL-6， and IL-1β in BALF were significantly elevated （P<0.01）. Histopathological analysis of lung tissue showed significant inflammatory infiltration， tissue edema， alveolar septal thickening， and apoptosis of lung tissue. Pronounced increases were observed in the mRNA expression levels of p38 MAPK， NF-κB p65， inhibitor of NF-κB （IκBα）， B-cell lymphoma-2 associated x protein （Bax）， and Caspases-3， as well as the protein expression levels of p-p38 MAPK， p-NF-κB p65， p-IκBα， Bax， Caspases-3， and cleaved Caspases-3， while the mRNA and protein expression of Bcl-2 was downregulated （P<0.01）. Compared with the model group， MKD significantly elevated PaO₂， SaO₂， and PaO₂/FiO₂ while reducing PaCO₂ and W/D ratio in rats （P<0.01）. It also greatly reduced TNF-α， IL-6， and IL-1β levels in BALF （P<0.01） and alleviated inflammatory infiltration， tissue edema， alveolar septal thickening， and apoptosis of lung tissue. Additionally， it downregulated the mRNA expression of p38 MAPK， NF-κB p65， IκBα， Bax， Caspases-3， as well as protein expression of p-p38 MAPK， p-NF-κB p65， p-IκBα， Bax， Caspases-3， and cleaved Caspases-3 in lung tissue （P<0.05， P<0.01）， while significantly upregulating mRNA and protein expression of Bcl-2 （P<0.01）. ConclusionMKD exerts a protective effect on OA-induced ALI rats， potentially through the regulation of the p38 MAPK/NF-κB signaling pathway to inhibit inflammation and apoptosis.

Pancreatic cancer is a kind of highly malignant tumor with a low survival rate and poor prognosis. The effectiveness of gemcitabine as a first-line chemotherapy drug is limited; however, it can activate dendritic cells and improve antigen presentation which increase the sensitivity of tumor cell to immunotherapy. Although immunotherapy has made some advancements in cancer treatment, the therapeutic benefit of programmed cell death receptor 1/programmed death receptor-ligand 1 (PD-1/PD-L1) blockade therapy remains relatively low. The chemokine C-X-C chemokine ligand 12 (CXCL12) contributes to an immunosuppressive tumor microenvironment by recruiting immunosuppressive cells. The receptor C-X-C motif chemokine receptor 4 (CXCR4), highly expressed in various tumors including pancreatic cancer, plays a crucial role in tumor development and progression. In this study, the anti-tumor immune response of human peripheral blood mononuclear cell (hPBMC) was enhanced using the combination of BsNb PX4 (anti-PD-L1&CXCR4 bispecific nanobody) and gemcitabine. In a co-culture system of gemcitabine-pretreated hPBMCs with tumor cells, the BsNb PX4 synergized gemcitabine to improve the cytotoxic activity of hPBMCs against tumor cells. Flow cytometry analysis confirmed increased ratio of CD8⁺ to CD4⁺ T cells in combination treatment. In NOD/SCID mice bearing pancreatic cancer, the combination treatment exhibited more infiltration of CD8⁺ T cells into tumor tissues, contributing to an effective anti-tumor response. This study presents potential new therapies for the treatment of pancreatic cancer. Ethical approval was obtained for collection of hPBMC samples from the Local Ethics Committee of Shanghai Jiao Tong University. All animal experiments were approved by the Animal Ethic Committee of Shanghai Jiao Tong University (authorizing number: A2024246).

Fecal microbiota transplantation (FMT) technology originated in China during the Eastern Jin Dynasty and has rapidly developed over the past two decades, becoming a primary method for studying the causal relationship between gut microbiota and the occurrence and progression of diseases. At the same time, the therapeutic effects of FMT in the field of gastrointestinal diseases have gained widespread recognition and are gradually expanding into other disease areas. The FMT procedure is relatively complex, and there is currently no standardized method; its success is influenced by various factors, including the donor, recipient, processing of the fecal material, and the method of implantation. Given the increasingly recognized relationship between gut microbiota and various diseases, FMT has become a research hotspot in both scientific studies and clinical applications, achieving a series of significant advancements. To help researchers better understand this technology, this paper will outline the development history of FMT, summarize common operational methods in research and clinical settings, review its application progress, and look forward to future development directions.

Atherosclerosis is a complex pathological condition resulting from lipid deposition， chronic inflammatory responses， and fibrosis， with a prolonged disease course and multifactorial etiology. Based on the traditional Chinese medicine （TCM） theory of accumulation syndrome， atherosclerosis can be classified under this category， with its pathogenesis involving phlegm， blood stasis， deficiency， and accumulation. This paper proposed a stage-based intervention strategy using the four therapeutic principles of "attacking， supplementing， dispersing， dissipating"， and divided into six stages based on the pathological progression， including the stage of accumulation before formation， the stage of accumulation already formed， the stage of nucleus accumulation， the stage of nucleus accumulation decay， the stage of nucleus accumulation consolidation， and the stage of severe stenosis of nucleus. At different stages， the intervention focuses on reinforcing healthy qi and consolidating the root， tonifying the kidneys and spleen， dispersing and removing turbidity， removing phlegm stagnation， promoting qi circulation， dispersing accumulations and removing stasis， attacking accumulation and expelling stasis， directing the turbid downward and dispersing accumulation， and treatment would be adjusted based on specific symptoms， which provides a theoretical framework for the prevention and treatment of atherosclerosis with TCM.

Platelet transfusion refractoriness (PTR) is a common issue among patients with hematological diseases and tumors. This article reviews the diagnostic criteria, influencing factors, and recent prevention and management strategies for immune PTR. The diagnostic criteria typically involve post-transfusion platelet increment (PI), platelet recovery rate (PPR), and corrected count increment (CCI). Both immune and non-immune factors can lead to PTR, with immune factors mainly including HLA and HPA antibodies. Prevention and management strategies include the use of leukocyte-reduced platelets, HLA and HPA antigen-matched platelets, intravenous immunoglobulin therapy, and immunosuppressive strategies. Although various strategies have been proposed and applied in clinical practice, the prevention and management of immune PTR remain challenging. Future research needs to explore more effective individualized treatment strategies, while also considering the potential application of emerging technologies such as nanotechnology in the field of transfusion.

In recent years, due to the development of radiotherapy technology and nuclear energy, people have paid more and more attention to the various effects of ionizing radiation on organisms. Ionizing radiation can induce protein, DNA and other biological macromolecules to damage, resulting in apoptosis, senescence, cancer and a series of changes. For a long time, it has been believed that the main target of ionizing radiation damage is DNA in the nucleus. However, it has been reported in recent years that ionizing radiation has both direct and indirect effects, and the theory of ROS damage in the indirect effects believes that ionizing radiation has target uncertainty, so it is not comprehensive enough to evaluate only the DNA damage in the nucleus. It has been reported that ionizing radiation can cause damage to organelles as well as damage to cells. Mitochondria are important damaged organelles because mitochondria occupy as much as 30% of the entire cell volume in the cytoplasm, which contains DNA and related enzymes that are closely related to cellular ATP synthesis, aerobic respiration and other life activities. What is more noteworthy is that mitochondria are the only organelles in which DNA exists in the human body, which makes researchers pay attention to various damage to mitochondrial DNA caused by ionizing radiation (such as double-strand breaks, base mismatching, and fragment loss). Although these damages also occur in the nucleus, mitochondrial DNA is more severely damaged than nuclear DNA due to its lack of histone protection, so mitochondria are important targets of ionizing radiation damage in addition to the nucleus. Mitochondrial DNA is not protected by histones and has little repair ability. When exposed to ionizing radiation, common deletions occur at an increased frequency and are passed on to offspring. For large-scale mitochondrial DNA damage, mitochondria indirectly compensate for the amount of damaged DNA by increasing the number of DNA copies and maintaining the normal function of mitochondrial DNA. Mitochondria are in a state of oxidative stress after exposure to ionizing radiation, and this oxidative stress will promote the change in mitochondrial function. When mitochondria are damaged, the activity of proteins related to aerobic respiration decreases, and oxidative respiration is inhibited to a certain extent. At the same time, a large amount of active superoxide anions are continuously produced to stimulate mitochondrial oxidative stress, and the signal of such damage is transmitted to the surrounding mitochondria, resulting in a cascade of damage reaction, which further activates the signalling pathway between mitochondria and nucleus. The cell nucleus is also in a state of oxidative stress, and finally, the level of free radicals is high, causing secondary damage to the genetic material DNA of mitochondria and nucleus. In this paper, the damage effects of ionizing radiation on mitochondria are reviewed, to provide a new idea for radiation protection.

Fibrosis, the pathological scarring of vital organs, is a severe and often irreversible condition that leads to progressive organ dysfunction. It is particularly pronounced in organs like the liver, kidneys, lungs, and heart. Despite its clinical significance, the full understanding of its etiology and complex pathogenesis remains incomplete, posing substantial challenges to diagnosing, treating, and preventing the progression of fibrosis. Among the various molecular players involved, platelet-derived growth factor-C (PDGF-C) has emerged as a crucial factor in fibrotic diseases, contributing to the pathological transformation of tissues in several key organs. PDGF-C is a member of the PDGFs family of growth factors and is synthesized and secreted by various cell types, including fibroblasts, smooth muscle cells, and endothelial cells. It acts through both autocrine and paracrine mechanisms, exerting its biological effects by binding to and activating the PDGF receptors (PDGFRs), specifically PDGFRα and PDGFRβ. This binding triggers multiple intracellular signaling pathways, such as JAK/STAT, PI3K/AKT and Ras-MAPK pathways. which are integral to the regulation of cell proliferation, survival, migration, and fibrosis. Notably, PDGF-C has been shown to promote the proliferation and migration of fibroblasts, key effector cells in the fibrotic process, thus accelerating the accumulation of extracellular matrix components and the formation of fibrotic tissue. Numerous studies have documented an upregulation of PDGF-C expression in various fibrotic diseases, suggesting its significant role in the initiation and progression of fibrosis. For instance, in liver fibrosis, PDGF-C stimulates hepatic stellate cell activation, contributing to the excessive deposition of collagen and other extracellular matrix proteins. Similarly, in pulmonary fibrosis, PDGF-C enhances the migration of fibroblasts into the damaged areas of lungs, thereby worsening the pathological process. Such findings highlight the pivotal role of PDGF-C in fibrotic diseases and underscore its potential as a therapeutic target for these conditions. Given its central role in the pathogenesis of fibrosis, PDGF-C has become an attractive target for therapeutic intervention. Several studies have focused on developing inhibitors that block the PDGF-C/PDGFR signaling pathway. These inhibitors aim to reduce fibroblast activation, prevent the excessive accumulation of extracellular matrix components, and halt the progression of fibrosis. Preclinical studies have demonstrated the efficacy of such inhibitors in animal models of liver, kidney, and lung fibrosis, with promising results in reducing fibrotic lesions and improving organ function. Furthermore, several clinical inhibitors, such as Olaratumab and Seralutinib, are ongoing to assess the safety and efficacy of these inhibitors in human patients, offering hope for novel therapeutic options in the treatment of fibrotic diseases. In conclusion, PDGF-C plays a critical role in the development and progression of fibrosis in vital organs. Its ability to regulate fibroblast activity and influence key signaling pathways makes it a promising target for therapeutic strategies aiming at combating fibrosis. Ongoing research into the regulation of PDGF-C expression and the development of PDGF-C/PDGFR inhibitors holds the potential to offer new insights and approaches for the diagnosis, treatment, and prevention of fibrotic diseases. Ultimately, these efforts may lead to the development of more effective and targeted therapies that can mitigate the impact of fibrosis and improve patient outcomes.

ObjectiveAs a second messenger in intracellular signal transduction, Ca²⁺ plays an important role in cell migration. Previous studies have demonstrated that extracellular Ca²⁺ influx can promote electric field-guided cell migration, known as electrotaxis. However, the effect of intracellular Ca²⁺ flow on electrotaxis is unclear. Therefore, in this study, we investigate the effect of Ca²⁺ flux on the electrotaxis of Dictyostelium discoideum. MethodsThe electrotaxis of Dictyostelium discoideum was investigated by applying a direct current (DC) electric field. Cell migration was recorded using a real-time imaging system. Calcium channel inhibitors, the extracellular Ca²⁺ chelator EGTA, Ca²⁺-free DB buffer, and caffeine were applied to investigate the impact of intra- and extracellular Ca²⁺ flow on electrotaxis. The involvement of G proteins and ERK2 in directed cell migration mediated by endoplasmic reticulum Ca²⁺ release was explored using mutants. ResultsDictyostelium discoideum migrated toward the cathode in the electric field in a voltage-dependent manner. The intracellular Ca²⁺ concentration of the cells was significantly increased in the electric field. Inhibition of both extracellular Ca²⁺ influx and intracellular Ca²⁺ release suppressed cell electrotaxis migration. Inhibition of endoplasmic reticulum Ca²⁺ release induced by caffeine significantly impaired the electrotaxis of Dictyostelium discoideum. Deletion of Gα2, Gβ, Gγ, and Erk2 notably reduced the electrotaxis of the cells. Enhancing Ca²⁺ release mediated by caffeine restored the electrotaxis of the Gα2^-, Gβ ^-, and Erk2^- mutant cells partially or completely, but did not restore electrotaxis in the Gγ^- mutant cells. ConclusionCa²⁺ release from the endoplasmic reticulum regulates electrotaxis migration in Dictyostelium discoideum and is involved in the regulation of cell electrotaxis by G proteins and ERK2.