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.

The official implementation of the Regulations on Clinical Research and Translation of New Biomedical Technologies (State Council Decree No.818, hereinafter referred to as the "Regulations") marks a new stage of legal governance, standardization, and whole-chain regulation for emerging biomedical fields such as cell and gene therapy (CGT) in China, exerting a profound impact on the development of transfusion medicine as a discipline. Within the framework of the core regulatory systems established by the Regulations, and drawing upon the extensive experience of transfusion medicine in comprehensive quality control, cell processing and handling, ethical compliance, and clinical translation, this study systematically elucidates the intrinsic alignment between transfusion medicine and CGT with respect to technical workflows, quality control rationale, and management systems. It further clarifies the discipline-specific advantages of the department of transfusion medicine to proactively undertake CGT engagement, while analyzing current shortcomings and transformational bottlenecks. By leveraging the existing institutional framework, the department of transfusion medicine is well positioned to evolve into a core platform for whole-process quality control and a pivotal hub for in-hospital clinical translation of CGT. However, this transformation must concurrently address multiple challenges, including heightened compliance responsibilities, lagging technical infrastructure, a shortage of interdisciplinary talent, and increasingly stringent standards for clinical research and translation. The Regulations provide a legal basis and policy support for the department of transfusion medicine to transcend its traditional, singular function of blood safety assurance and establish a synergistic development model integrating blood safety and cell therapy. Therefore, the department of transfusion medicine should proactively align with regulatory requirements, refine whole-process compliance systems, upgrade technical platforms, and cultivate interdisciplinary professionals to achieve high-quality transformative development as a core supporting discipline for biotherapy.

BACKGROUND:The phosphatidylinositol 3-kinase/protein kinase(PI3K/AKT)signaling pathway plays a pivotal role in regulating osteoclast activation,which is essential for maintaining bone homeostasis.Bone destruction in osteoarticular tuberculosis is caused by aberrant osteoclastogenesis induced by Mycobacterium tuberculosis infection.However,the role of the PI3K signaling pathway in Mycobacterium tuberculosis-induced aberrant osteoclastogenesis remains unclear. OBJECTIVE:To investigate the effects and mechanisms of the PI3K/AKT signaling pathway inhibitor BYL-719 on aberrant osteoclastogenesis induced by Mycobacterium tuberculosis. METHODS:RAW264.7 cells were infected with bovine Mycobacterium tuberculosis bacillus calmette-cuerin vaccine,and Ag85B was used for cellular immunofluorescence staining.The cell counting kit-8 assay was employed to determine the safe concentration of BYL-719.There were four groups in the experiment:blank control group,BYL-719 group,BCG group,and BCG+BYL-719 group.Under the induction of receptor activator of nuclear factor kappa-B ligand,the effects of BYL-719 on post-infection osteoclast differentiation and fusion were explored through tartrate-resistant acid phosphatase staining and phalloidin staining.RT-PCR and western blot were used to detect the expression of osteoclast-related genes and proteins,and further investigate the mechanism of action. RESULTS AND CONCLUSION:Immunofluorescence staining showed that RAW264.7 cells phagocytosed Mycobacterium tuberculosis.Cell counting kit-8 data indicated that 40 nmol/L BYL-719 was non-toxic to cells.Tartrate-resistant acid phosphatase staining and phalloidin staining showed that BYL-719 inhibited the generation and fusion ability of osteoclasts following infection.RT-PCR and western blot results also indicated that BYL-719 suppressed the upregulation of osteoclast-specific genes(including c-Fos,NFATc1,matrix metalloproteinase 9,and CtsK)induced by Mycobacterium tuberculosis infection(P<0.05).Western blot and immunofluorescence staining revealed that BYL-719 inhibited excessive osteoclast differentiation induced by Mycobacterium tuberculosis by downregulating the expression of IκBα-p65.To conclude,BYL-719 inhibits aberrant osteoclastogenesis induced by Mycobacterium tuberculosis through the downregulation of IκBα/p65.Therefore,the IκBα/p65 signaling pathway is a potential therapeutic target for osteoarticular tuberculosis,and BYL-719 holds potential value for the preventing and amelioration of bone destruction in osteoarticular tuberculosis.BYL-719 has the potential to prevent and ameliorate bone destruction in osteoarticular tuberculosis.

OBJECTIVE To explore the mechanism by which Cuscuta chinensis flavonoids （CCF） promote decidualization and improve recurrent spontaneous abortion （RSA）. METHODS HTR-8/SVneo cells in logarithmic growth phase were randomly divided into blank group， lipopolysaccharide （LPS） group， CCF group， SGK2 inhibitor （GSK650394， abbreviated as “GSK”） group and CCF+GSK group. Each group was treated with the corresponding agents accordingly. HTR-8/SVneo cells with SGK2 knockdown were randomly divided into small interfering RNA of SGK2 （siSGK2） group and siSGK2+CCF group； additionally， blank group and LPS group were established； each group was treated with the corresponding agents accordingly. The cell survival rate， expression levels of WNK signaling pathway- and decidualization-related proteins and mRNAs， as well as mitochondrial membrane potential levels， were assessed in each group before and after SGK2 knockdown. RSA mice model was constructed and randomly divided into model group， CCF low-dose group， CCF high-dose group， GSK group， and combined dosing group， with 4 mice in each group. Other 4 normal pregnant female mice were selected as the control group. The number of implanted embryos， viable fetuses， and lost embryos in mice was recorded. The morphological changes of endometrium and decidualization were observed， and WNK signaling pathway- and decidualization-related proteins and mRNAs expressing levels as well as mitochondrial membrane potential levels were all detected. RESULTS Compared with the blank group， the cell survival rate， as well as the protein and mRNA expression levels of SGK2， WNK1， WNK4， prolactin， insulin-like growth factor- binding protein-1， oxidative stress responsive kinase 1， and Ste20-like proline-/alanine-rich kinase were significantly reduced in the LPS group （P＜0.05）； compared with the LPS group， the cell survival rate and the expression levels of the above- mentioned proteins and mRNAs were significantly increased in the CCF group， while the cell survival rate and the expression levels of the above-mentioned proteins and mRNAs were significantly decreased in the GSK group （P＜0.05）； compared with the CCF group， the cell survival rate and the expression levels of the above-mentioned proteins and mRNAs were significantly reduced in the CCF+GSK group （P＜0.05）. After knocking down SGK2， compared with the LPS group， the cell survival rate， red/green fluorescence intensity ratio， and the expression levels of the above-mentioned proteins and mRNAs were significantly reduced in the siSGK2 group （P＜0.05）； compared with the siSGK2 group， the cell survival rate， red/green fluorescence intensity ratio， and the expression levels of the above-mentioned proteins and mRNAs were significantly increased in the siSGK2+CCF group （P＜0.05）. The in vivo experimental results showed that CCF treatment can significantly improve the number of implanted embryos and viable fetuses in RSA model mice and reduce lost embryos， the expression levels of the above-mentioned proteins and mRNAs in endometrial tissue were significantly increased， and the red/green fluorescence intensity ratio was significantly increased （P＜ 0.05）； the combined dosing group could reverse the effect of CCF （P＜0.05）. CONCLUSIONS CCF can activate SGK2， up- regulate the WNK signaling pathway， promote endometrial decidualization， and improve RSA.

Objective: To analyze the change trends in the body shape indicators and proportions of students in Harbin from 2010 to 2024, and to investigate ergonomic compatibility of functional dimensions of school desks and chairs with current student shape indicators, so as to provide a reference for revising furniture standards of desks and chairs. Methods: Between September and November of both 2010 and 2024, a combination of convenience sampling and stratified cluster random sampling was conducted across three districts in Harbin, yielding samples of 6 590 and 6 252 students, respectively. Anthropometric shape indicators cluding height, sitting height, crus length, and thigh length-and their proportional changes were compared over the 15-year period. The 2024 data were compared with current standard functional dimensions of school furniture. The statistical analysis incorporated t-test and Mann-Whitney U- test. Results: From 2010 to 2024, average height increased by 1.8 cm for boys and 1.5 cm for girls; sitting height increased by 1.5 cm for both genders; crus length increased by 0.3 cm for boys and 0.4 cm for girls; and thigh length increased by 0.5 cm for both genders. The ratios of sitting height to height, and sitting height to leg length increased by less than 0.1 . The difference between desk chair height and 1/3 sitting height ranged from 0.4-0.8 cm. Among students matched with size 0 desks and chairs, 22.0% had a desk to chair height difference less than 0, indicating that the desk to chair height difference might be insufficient for taller students. The differences between seat height and fibular height ranged from -1.4 to 1.1 cm; and the differences between seat depth and buttock popliteal length ranged from -9.8 to 3.4 cm. Among obese students, the differences between seat width and 1/2 hip circumference ranged from -20.5 to -8.7 cm, while it ranged from -12.2 to -3.8 cm among non obese students. Conclusion Current furniture standards basically satisfy hygienic requirements; however, in the case of exceptionally tall and obese students, ergonomic accommodations such as adaptive seating allocation or personalized adjustments are recommended to meet hygienic requirements.

Objective:To discuss the protective effect of TUG-891 on ischemic stoke(IS)induced by ischemia-hypoxia,and to clarify its potential mechanism.Methods:A total of 60 healthy male C57BL/6 mice were randomly divided into sham operation group(n=20),model group[distal middle cerebral artery occlusion(dMCAO)group,n=20],and model+TUG-891 group(dMCAO+TUG-891 group,n=20).After modeling,the mice were intraperitoneally injected with TUG-891 solution(35 mg·kg?1·d?1)for 3 consecutive days.Modified neurological severity score(mNSS)and rotarod test were used to evaluate the neurological function of the mice in various groups;2,3,5-triphenyltetrazolium chloride(TTC)staining was used to observe the cerebral infarction volumes of the mice in various groups;biochemical method was used to detect the malondialdehyde(MDA)level and superoxide dismutase(SOD)activity in the supernatant of brain tissue of the mice in various groups;Hematoxylin-Eosin(HE)and NISSL staining were used to observe the pathomerphology of brain tissue of the mice in various groups;terminal deoxynucleotidyl transferase dUTP nick-end labeling(TUNEL)staining was used to detect the apoptotic indexes of neuronal cells in brain tissue of the mice in various groups;Western blotting method was used to detect the expression levels of glucose-regulated protein 78(GRP78),protein kinase R-like endoplasmic reticulum kinase(PERK),phosphorylated PERK(p-PERK),and C/EBP homologous protein(CHOP)proteins in brain tissue of the mice in various groups.Results:The mNSS and rotarod test results shoued that compared with sham operation group,the mNSS of the mice in dMCAO group was significantly increased(P<0.01),and the time on the rod was significantly decreased(P<0.01);compared with dMCAO group,the mNSS of the mice in dMCAO+TUG-891 group was decreased(P<0.05),and the time on the rod was increased(P<0.05).The TTC staining results shoued that compared with sham operation group,the volume of white infarct foci in the cerebral cortex of the mice in dMCAO group was increased(P<0.01);compared with dMCAO group,the cerebral infarction volume of the mice in dMCAO+TUG-891 group was significantly decreased(P<0.01).The HE staining results showed that compared with sham operation group,the cortex of the mice in dMCAO group was severely damaged,manifested by disordered arrangement of neuronal cells and obvious nuclear pyknosis in the infarct area,and the morphology of cortical infarct area of the mice in dMCAO+TUG-891 group was improved;the NISSL staining results showed that the Nissl bodies in the cortical infarct area of the mice in dMCAO group became thinner,elongated,and lost more.The pathological damage of brain tissue of the mice in dMCAO+TUG-891 group was significantly improved.Compared with sham operation group,the MDA level in brain tissue of the mice in model group was significantly increased(P<0.01),and the SOD activity was decreased(P<0.01);compared with model group,the MDA level in brain tissue of the mice in TUG-891 group was significantly decreased(P<0.01),and the SOD activity was significantly increased(P<0.01).The TUNEL staining results showed that compared with sham operation group,the apoptotic index of neuronal cells in brain tissue of the mice in dMCAO group was increased(P<0.01);compared with dMCAO group,the apoptotic index of neuronal cells in brain tissue of the mice in dMCAO+TUG-891 group was decreased(P<0.01).Compared with sham operation group,the expression levels of GRP78,p-PERK,and CHOP proteins in brain tissue of the mice in dMCAO group were increased(P<0.05);compared with dMCAO group,the expression levels of GRP78,p-PERK,and CHOP proteins in brain tissue of the mice in dMCAO+TUG-891 group were decreased(P<0.05).Conclusion:TUG-891 can alleviate neurological injury caused by ischemic stroke,and its mechanism may be related to the inhibition of endoplasmic reticulum stress and apoptosis.

As a type of acute cerebrovascular disease,stroke is one of the most common fatal and disabling diseases in the world,which seriously threatens the quality of life of patients;however,there are still limited treatment methods for this disease in clinical practice.Traditional Chinese medicine(TCM)has a long history and good efficacy in the treatment of stroke,and the active components of TCM can alleviate nerve injury caused by stroke by improving the development and progression of various pathophysiological mechanisms such as nerve inflammation,oxidative stress,and blood-brain barrier damage.This article reviews the role of active components of TCM in the treatment of ischemic stroke,in order to provide more ideas and options for the clinical treatment of this disease in the future.

Objective To investigate the number and categories of cognitive subtypes in individuals with First-Episode Schizophrenia(FES)and to explore the potential neurobiological sleep characteristics associated with these distinct cognitive subtypes.Methods The cognitive functions of 45 patients withFES and 40 healthy controls(HCs)were assessed using the MATRICS Consensus Cognitive Battery(MCCB).Latent profile analysis was employed to identify and classify the cognitive subtypes of FES patients.Furthermore,a full-night polysom-nographic recording was conducted to quantify the characteristics of sleep spindle waves.Subsequently,differ-ences in sleep spindle wave features among the identified cognitive subtypes of FES were analyzed and compared.Results Latent Profile Analysis identified two cognitive subtypes among FES patients:a subtype characterized by severe cognitive impairment(SIS,n=32)and another with relatively preserved cognitive function(CRP,n=13).Compared to healthy controls(HCs,n=40),FES patients exhibited increased spindle wave amplitude dur-ing both N2 and N3 sleep stages.Further analysis revealed that the spindle wave duration during the N2 stage was significantly longer in the SIS subtype compared to both CRP and HCs.Similarly,in the N3 stage,the spindle wave duration was longer in SIS than in CRP.Additionally,spindle wave frequency during the N3 stage was higher in both SIS and HCs compared to CRP.Conclusions The results of this study suggest that variations in the fre-quency and duration of spindle waves among different cognitive subtypes may serve as potential neurobiological markers for distinguishing FES cognitive subtypes.

Objective To understand the economic losses due to healthcare-associated infection(HAI)in patients after Da Vinci robotic thoracic surgery,and provide basis for preventing and controlling HAI after robotic surgery.Methods Patients who underwent Da Vinci robotic surgery from April 2019 to April 2023 were retrospective stu-died.Patients were divided into HAI group and non-HAI group based on the occurrence of postoperative infection.Through 1∶1 propensity score matching(PSM),31 cases were included in each group,economic losses of two groups of patients were compared.Results A total of 921 patients who underwent Da Vinci robotic thoracic surgery were included in the study,51 cases with HAI(HAI group)and 870 without HAI(non-HAI group).After 1∶1 PSM,31 cases were included in each group.Four covariates were compared between two groups of patients before PSM,namely gender,age,comorbidities,and the American Society of Anesthesiologists(ASA)grading,all with statistically significant differences(all P＜0.05).After PSM,distribution of the above covariates reached equilib-rium between the two groups(both P＞0.05).The median total expense for HAI group before PSM during hospi-talization was 88 711.72 Yuan,while 78 509.46 Yuan for the non-HAI group.The direct economic losses caused by HAI after Da Vinci robot surgery was 10 202.26 Yuan,mainly increased by expense of medicine,nursing,laborato-ry diagnosis,etc.Difference in western medicine expense was the highest(8 839.12 Yuan),out of which expense of antimicrobial agents accounted for the highest proportion(73.55％).Difference in daily hospitalization expense between HAI-group and non-HAI group was 502.38 Yuan.Length of hospital stay of patients in HAI group and non-HAI group were(21.59±10.62)and(13.92±9.21)days,respectively,with statistical differences(all P＜0.05).Conclusion The occurrence of HAI in patients undergoing Da Vinci robotic thoracic surgery leads to direct economic losses,with obvious increases in expenses of nursing,laboratory diagnosis,western medicine(mainly an-timicrobial agents).Length of hospital stay of patients also prolongs.

Objective:To investigate the protective effect of prunetin on the neurons in the rats with cerebral ischemia reperfusion injury(CIRI),and to clarify its possible mechanisms.Methods:Thirty-six SD rats were randomly divided into sham operation group,model group,low dose of prunetin group(3.5 mg·kg-1),medium dose of prunetin group(7.0 mg·kg-1),high dose of prunetin group(14.0 mg·kg-1),and positive drug edaravone(Eda)group(n=6).Zealonga method was used to evaluate the neurological function damage of the rats in various groups;open field experiment was used to evaluate the autonomous motor function;Triphenyltetrazolium chlorde(TTC)staining was used to evaluate the areas of cerebral infarction of the rats in various groups;HE staining and Nissl staining were used to observe the pathomorphology of brain tissue of the rats in various groups.Additionally,twenty-one SD rats were randomly divided into sham operation group,model group,prunetin group,c-Jun N-terminal kinase(JNK)inhibitor group,p38 inhibitor group,JNK inhibitor+prunetin group,and p38 inhibitor+prunetin group(n=3).TUNEL staining was used to detect the positive rates of apoptosis of neurons of the rats in various groups;Western blotting method was used to detect the expression levels of apoptosis-related proteins and JNK/p38 signaling pathway-related proteins in brain tissue of cerebral infarction side of the rats in various groups.Results:Compared with sham operation group,the neurological deficit score of rats in model group was significantly increased(P＜0.001),the total motor distance was shortened(P＜0.001),and the ratio of cerebral infarction area was increased(P＜0.001).In sham group,the neuronal structure in the rat brain tissue was clear and well-organized,with an abundance of Nissl bodies and no apparent pathological changes observed.Compared with model group,the neurological deficit scores of the rats in medium and high doses of prunetin groups were decreased(P＜0.05),total motor distances of rats were increased(P＜0.05),and the cerebral infarction areas of rats were decreased(P＜0.05);the neurons showed disarrayed arrangement,cytoplasmic condensation,nuclear consolidation,and lysing and deletion of Nissl bodies were decreased.Compared with sham operation group,the positive rate of apoptosis of neurons in model group was significantly increased(P＜0.001),the expression level of B-cell lymphoma-2(Bcl-2),Bcl-2-associated X protein(Bax)and cleaved Caspase-3 proteins in brain tissue of the rats were significantly increased(P＜0.05 or P＜0.01).Compared with model group,the positive rats of apoptosis of neurons of the rats in prunetin group were decreased(P＜0.05),the expression level of Bcl-2 protein in brain tissue of the rats was increased(P＜0.001),and the expression levels of Bax and cleaved Caspase-3 proteins were significantly decreased(P＜0.05).Compared with inhibitor groups,the positive rates of apoptosis of neurons in inhibitor+prunetin groups were decreased(P＜0.01),and the expression levels of p-JNK and p-p38 proteins in brain tissue of the rats as well as the ratios of p-JNK/JNK and p-p38/p38 were decreased(P＜0.05).Conclusion:Prunetin has the effect of reducing the neurological function damage,decreasing the area of cerebral infarction,reducing the pathological damage,and inhibiting neuronal apoptosis in the rats,and its mechanism may be related to inhibiting neuronal apoptosis through regulating the JNK/p38 signaling pathway.