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.

Objective To investigate the genetic characteristics of the VP1 region of Coxsackievirus A10 (CVA10) in Yunnan Province. Methods Fecal samples of suspected hand, foot and mouth disease (HFMD) were subjected to real-time fluorescent quantitative PCR for detection of enterovirus CVA10. Positive samples were subjected to VP1 gene sequence amplification and Sanger sequencing. Sequence splicing was performed with DNAstar7.1 Seqman software, and nucleotide sequence and amino acid site analysis were performed using Mega 6.0 software. Results The sequencing of VP1 gene of CVA10 obtained a sequence of 894 nucleotides, encoding 298 amino acids. Compared with the original strain, there were mainly three active amino acid mutation regions, 13-33, 141-142, and 283-285. The nucleotide difference rate between the Yunnan isolates and the reference strain ranged from 16.92% to 30.90%, and the amino acid difference rate ranged from 2.58% to 4.00%. C1 and C2 group nucleotide difference was 10.58%, and the amino acid difference rate was 1.80%. The VP1 150-176 region exhibited highly conserved characteristics. Six CVA10 strains and Sichuan strain MW178898 belonged to the C1 group of the C genotype. The other 14 CVA10 strains belonged to the C2 group. Conclusion VP1 gene mutation is active and CVA10 is an important pathogen of HFMD in Yunnan. C2 genotype of CVA10 is dominant in this study, and C1 and C2 have co-circulated in Yunnan. It is necessary to strengthen monitoring and develop multivalent vaccines containing CVA10 epidemic genotype.

OBJECTIVE: To evaluate the effect of biodegradable magnesium alloy materials in promoting tendon-bone healing during rotator cuff tear repair and to investigate their potential underlying biological mechanisms. METHODS: Forty-eight 8-week-old Sprague Dawley rats were taken and randomly divided into groups A, B, and C. Rotator cuff tear models were created and repaired using magnesium alloy sutures in group A and Vicryl Plus 4-0 absorbable sutures in group B, while only subcutaneous incisions and sutures were performed in group C. Organ samples of groups A and B were taken for HE staining at 1 and 2 weeks after operation to evaluate the safety of magnesium alloy, and specimens from the supraspinatus tendon and proximal humerus were harvested at 2, 4, 8, and 12 weeks after operation. The specimens were observed macroscopically at 4 and 12 weeks after operation. Biomechanical tests were performed at 4, 8, and 12 weeks to test the ultimate load and stiffness of the healing sites in groups A and B. At 2, 4, and 12 weeks, the specimens were subjected to the following tests: Micro-CT to evaluate the formation of bone tunnels in groups A and B, HE staining and Masson staining to observe the regeneration of fibrocartilage at the tendon-bone interface after decalcification and sectioning, and Goldner trichrome staining to evaluate the calcification. Immunohistochemical staining was performed to detect the expressions of angiogenic factors, including vascular endothelial growth factor (VEGF) and bone morphogenetic protein 2 (BMP-2), as well as osteogenic factors at the tendon-bone interface. Additionally, immunofluorescence staining was used to examine the expressions of Arginase 1 and Integrin beta-2 to assess M1 and M2 macrophage polarization at the tendon-bone interface. The role of the phosphatidylinositol 3-kinase (PI3K)/protein kinase B (AKT) signaling pathway in tendon-bone healing was further analyzed using real-time fluorescence quantitative PCR. RESULTS: Analysis of visceral sections revealed that magnesium ions released during the degradation of magnesium alloys did not cause significant toxic effects on organs such as the heart, liver, spleen, lungs, and kidneys, indicating good biosafety. Histological analysis further demonstrated that fibrocartilage regeneration at the tendon-bone interface in group A occurred earlier, and the amount of fibrocartilage was significantly greater compared to group B, suggesting a positive effect of magnesium alloy material on tendon-bone interface repair. Additionally, Micro-CT analysis results revealed that bone tunnel formation occurred more rapidly in group A compared to group B, further supporting the beneficial effect of magnesium alloy on bone healing. Biomechanical testing showed that the ultimate load in group A was consistently higher than in group B, and the stiffness of group A was also greater than that of group B at 4 weeks, indicating stronger tissue-carrying capacity following tendon-bone interface repair and highlighting the potential of magnesium alloy in enhancing tendon-bone healing. Immunohistochemical staining results indicated that the expressions of VEGF and BMP-2 were significantly upregulated during the early stages of healing, suggesting that magnesium alloy effectively promoted angiogenesis and bone formation, thereby accelerating the tendon-bone healing process. Immunofluorescence staining further revealed that magnesium ions exerted significant anti-inflammatory effects by regulating macrophage polarization, promoting their shift toward the M2 phenotype. Real-time fluorescence quantitative PCR results demonstrated that magnesium ions could facilitate tendon-bone healing by modulating the PI3K/AKT signaling pathway. CONCLUSION Biodegradable magnesium alloy material accelerated fibrocartilage regeneration and calcification at the tendon-bone interface in rat rotator cuff tear repair by regulating the PI3K/AKT signaling pathway, thereby significantly enhancing tendon-bone healing.
Animals ; Rotator Cuff Injuries/metabolism* ; Rats, Sprague-Dawley ; Signal Transduction ; Wound Healing/drug effects* ; Alloys/pharmacology* ; Rats ; Proto-Oncogene Proteins c-akt/metabolism* ; Rotator Cuff/metabolism* ; Macrophages/metabolism* ; Magnesium/pharmacology* ; Phosphatidylinositol 3-Kinases/metabolism* ; Vascular Endothelial Growth Factor A/metabolism* ; Male ; Biocompatible Materials ; Bone Morphogenetic Protein 2/metabolism*

Neuropathic pain is frequently comorbidity with cognitive deficits. Neuralized1 (Neurl1)-mediated ubiquitination of CPEB3 in the hippocampus is critical in learning and memory. However, the role of Neurl1 in the cognitive impairment in neuropathic pain remains elusive. Herein, we found that lumbar 5 spinal nerve ligation (SNL) in male rat-induced neuropathic pain was followed by learning and memory deficits and LTP impairment in the hippocampus. The Neurl1 expression in the hippocampal CA1 was decreased after SNL. And this decrease paralleled the reduction of ubiquitinated-CPEB3 level and reduced production of GluA1 and GluA2. Overexpression of Neurl1 in the CA1 rescued cognitive deficits and LTP impairment, and reversed the reduction of ubiquitinated-CPEB3 level and the decrease of GluA1 and GluA2 production following SNL. Specific knockdown of Neurl1 or CPEB3 in bilateral hippocampal CA1 in naïve rats resulted in cognitive deficits and impairment of synaptic plasticity. The rescued cognitive function and synaptic plasticity by the treatment of overexpression of Neurl1 before SNL were counteracted by the knockdown of CPEB3 in the CA1. Collectively, the above results suggest that the downregulation of Neurl1 through reducing CPEB3 ubiquitination and, in turn, repressing GluA1 and GluA2 production and mediating synaptic plasticity impairment in hippocampal CA1 leads to the genesis of cognitive deficits in neuropathic pain.
Animals ; Male ; Neuralgia/metabolism* ; Rats ; Down-Regulation/physiology* ; Ubiquitination/physiology* ; Neuronal Plasticity/physiology* ; Rats, Sprague-Dawley ; CA1 Region, Hippocampal/metabolism* ; Cognitive Dysfunction/metabolism* ; RNA-Binding Proteins/metabolism* ; Receptors, AMPA/metabolism*

Sepsis is a life-threatening organ dysfunction syndrome caused by a dysregulated host response to infection. Septic acute kidney injury (SAKI) is one of the most common complications of sepsis, and the occurrence of acute kidney injury (AKI) indicates that the patient's condition is critical with a poor prognosis. The traditional view holds that the main mechanism of SAKI is the reduction of renal blood flow, inadequate renal perfusion, inflammatory response, and microcirculatory dysfunction caused by sepsis, which subsequently leads to ischemia and necrosis of renal tubular cells. Recent research findings indicate that processes such as autophagy and other forms of programmed cell death play an increasingly important role. Autophagy is a programmed intracellular degradation process and is a form of programmed cell death. Cells degrade their cytoplasmic components via lysosomes, breaking down and recycling intracellular constituents to meet their metabolic needs, maintain intracellular homeostasis, and renew organelles. During SAKI, autophagy plays a crucial protective role through various mechanisms, including regulating inflammation and immune responses, clearing damaged organelles, and maintaining stability in the intracellular environment. In recent years, the role of autophagy in the pathogenesis and treatment of SAKI has received widespread attention. Research has confirmed that various intracellular signaling pathways and signaling molecules targeting autophagy [such as mammalian target of rapamycin (mTOR) signaling pathway, AMP-activated protein kinase (AMPK) signaling pathway, nuclear factor-κB (NF-κB) signaling pathway, and Sirtuins (SIRT), autophagy associated factor Beclin-1, and Toll-like receptor (TLR)] are involved in the development of SAKI. Due to the complex pathogenesis of SAKI, current treatment strategies include fluid management, infection control, maintenance of internal environment balance, and renal replacement therapy; however, the mortality remains high. In recent years, it has been found that autophagy plays a critical protective role in sepsis-mediated AKI. As a result, an increasing number of drugs are being developed to alleviate SAKI by regulating autophagy. This article reviews the latest advances in the role of autophagy in the pathogenesis and treatment of SAKI, with the aim of providing insights for the development of new drugs for SAKI patients.
Humans ; Acute Kidney Injury/etiology* ; Autophagy ; Sepsis/complications* ; Signal Transduction

ObjectiveTo investigate the effect of dapagliflozin on liver lipid metabolism and gut microecology in mice with metabolic associated fatty liver disease （MAFLD）， and to clarify its potential mechanism. MethodsA total of 50 male C57 mice were randomly divided into Control group， type 2 diabetes+MAFLD group （MAFLD group）， dapagliflozin group （DAPA group）， meldonium group （THP group）， and dapagliflozin+meldonium group （DAPA+THP group）， with 10 mice in each group. High-fat diet combined with streptozotocin was used to establish a mouse model of MAFLD. Treatment outcomes were assessed based on histopathology and biochemical parameters such as blood glucose and blood lipid levels， and the transcriptomic and metagenomic analyses were used to identify differentially expressed genes and the changes in gut microbiota. A one-way analysis of variance was used for comparison of normally distributed continuous data between multiple groups， and the least significant difference t-test was used for comparison between two groups； the Kruskal-Wallis H test was used for comparison of non-normally distributed continuous data between multiple groups， and the Nemenyi test was used for comparison between two groups. ResultsHistopathological examination showed that the mice in the MAFLD group had excessive lipid deposition and hepatocyte steatosis； compared with the MAFLD group， the DAPA group had a significant improvement in hepatocyte steatosis， while the THP group and the DAPA+THP group had a less significant improvement compared with the DAPA group. Compared with the Control group， the MAFLD group had a significant increase in fasting blood glucose （P<0.05）， significant increases in the serum levels of alanine aminotransferase （ALT）， aspartate aminotransferase （AST）， malondialdehyde， total cholesterol， triglyceride， and low-density lipoprotein cholesterol （P<0.05）， and a significant reduction in high-density lipoprotein cholesterol （P<0.05）. Compared with the MAFLD group， the DAPA group， the THP group， and the DAPA+THP group had significant reductions in the serum levels of ALT and AST （P<0.05）. The results of 16S rRNA sequencing showed that compared with the Control group， the MAFLD group had significant changes in gut microbiota， with an increase in Firmicutes and a reduction in Bacteroidetes， as well as reductions in S24-7 and Erysipelotrichaceae and an increase in Lactobacillaceae. The levels of the above flora were upregulated to normal levels in the DAPA group， the THP group， and the DAPA+THP group. The liver transcriptomic analysis showed that the enriched metabolic pathways included steroid hormone biosynthesis， bile secretion， inflammatory mediator regulation of TRP， fatty acid elongation， and lipid biodegradation processes， and the related genes mainly involved the key targets of lipid metabolism such as Acot2， Angptl4， Scd2， and Npc1l1. ConclusionDapagliflozin can alleviate MAFLD through the pathways such as steroid hormone biosynthesis， bile secretion， inflammatory mediator regulation of TRP， and fatty acid elongation， as well as by regulating gut microbiota homeostasis.

To investigate the strain composition and drug resistance characteristics of G +(Gram positive cocci) cocci causing bloodstream infections in the People′s Hospital of Inner Mongolia Autonomous Region in recent years and provide a basis for the empirical and rational use of drugs for the prevention and treatment of bloodstream infections caused by G +cocci. The strain composition and drug-resistant characteristics of G +cocci isolated from positive blood culture specimens sent to various departments of the Inner Mongolia Autonomous Region People′s Hospital from January 2015 to December 2022 were retrospectively analyzed, and the higher detection rates of Staphylococcus hominis and Staphylococcus epidermidis, Enterococcus faecium and Enterococcus faecalis, and methicillin-resistant Staphylococcus aureus (MRSA) and methicillin-sensitive Staphylococcus aureus (MSSA) were examined. MRSA and methicillin-sensitive Staphylococcus aureus (MSSA) were comparatively analyzed for resistance. The resistance data were analyzed by Whonet 5.6 statistical software, the significance of difference was analyzed by SPSS 22.0 software, and the resistance rate was compared by χ2 test. The results showed that 1 209 strains of G +cocci, in terms of the composition ratio, from high to low, were mainly human staphylococci (32.5%,393/1 209), Staphylococcus epidermidis (27.8%, 336/1 209), Staphylococcus aureus (14.9%,180/1 209) and Enterococcus faecalis (10.6%, 128/1 209). Among them, the detection rate of methicillin-resistant Staphylococcus aureus (MRSA) (42.8%, 77/180) was lower than that of methicillin-resistant coagulase-negative staphylococcus (MRCNS) (71.5%, 608/850); and among enterococci, the detection rate of Enterococcus faecalis (71.5%, 128/179) was much higher than that of Enterococcus faecalis (28.5%, 51/179). For drug resistance, the resistance rate to five commonly used antimicrobial drugs, ciprofloxacin, levofloxacin, moxifloxacin, clindamycin and tetracycline, was higher in Staphylococcus hominis than in Staphylococcus epidermidis ( χ2=7.152-64.080, P<0.05); however, for the aminoglycoside antimicrobial drug gentamicin, the rate of resistance in Staphylococcus humanus was lower than in Staphylococcus epidermidis, and the difference was statistically significant ( χ2=11.895, P<0.05); no strains resistant to linezolid and vancomycin were found in both. Comparison of the resistance rates to seven antimicrobial drugs, gentamicin, rifampicin, ciprofloxacin, levofloxacin, moxifloxacin, clindamycin and tetracycline, was significantly higher in MRSA than in MSSA ( χ2=6.169-56.941, P<0.05); however, the resistance rate to cotrimoxazole, MRSA (15.6%, 12/77) was significantly lower than that of MSSA (35.3%, 36/102), and the difference was statistically significant ( χ2=5.155, P<0.05); MRSA and MSSA resistant to linezolid and vancomycin were not found. The resistance rate of Enterococcus faecalis to penicillin G and ampicillin was much higher than that of Enterococcus faecalis, and the difference was statistically significant ( χ2=22.965, P<0.05), and vancomycin-resistant enterococci (VRE) were not found. In conclusion, for staphylococci, except for individual antibiotics, S.hominis and MRSA were more resistant to most antimicrobial drugs than S. epidermidis and MSSA, showing a multidrug-resistant pattern. For enterococci, except for penicillin G and ampicillin resistance rate, Enterococcus faecalis is much higher than Enterococcus faecalis, the rest of the antimicrobial drugs did not see a significant difference, in addition to vancomycin-resistant enterococci were not detected. Clinicians should pay great attention to the monitoring data of multidrug-resistant G +cocci isolated from blood cultures to provide a basis for empirical and rational use of drugs in the clinic, to effectively prevent and reduce the incidence of bloodstream infections caused by G +cocci.

To investigate the strain composition and drug resistance characteristics of G +(Gram positive cocci) cocci causing bloodstream infections in the People′s Hospital of Inner Mongolia Autonomous Region in recent years and provide a basis for the empirical and rational use of drugs for the prevention and treatment of bloodstream infections caused by G +cocci. The strain composition and drug-resistant characteristics of G +cocci isolated from positive blood culture specimens sent to various departments of the Inner Mongolia Autonomous Region People′s Hospital from January 2015 to December 2022 were retrospectively analyzed, and the higher detection rates of Staphylococcus hominis and Staphylococcus epidermidis, Enterococcus faecium and Enterococcus faecalis, and methicillin-resistant Staphylococcus aureus (MRSA) and methicillin-sensitive Staphylococcus aureus (MSSA) were examined. MRSA and methicillin-sensitive Staphylococcus aureus (MSSA) were comparatively analyzed for resistance. The resistance data were analyzed by Whonet 5.6 statistical software, the significance of difference was analyzed by SPSS 22.0 software, and the resistance rate was compared by χ2 test. The results showed that 1 209 strains of G +cocci, in terms of the composition ratio, from high to low, were mainly human staphylococci (32.5%,393/1 209), Staphylococcus epidermidis (27.8%, 336/1 209), Staphylococcus aureus (14.9%,180/1 209) and Enterococcus faecalis (10.6%, 128/1 209). Among them, the detection rate of methicillin-resistant Staphylococcus aureus (MRSA) (42.8%, 77/180) was lower than that of methicillin-resistant coagulase-negative staphylococcus (MRCNS) (71.5%, 608/850); and among enterococci, the detection rate of Enterococcus faecalis (71.5%, 128/179) was much higher than that of Enterococcus faecalis (28.5%, 51/179). For drug resistance, the resistance rate to five commonly used antimicrobial drugs, ciprofloxacin, levofloxacin, moxifloxacin, clindamycin and tetracycline, was higher in Staphylococcus hominis than in Staphylococcus epidermidis ( χ2=7.152-64.080, P<0.05); however, for the aminoglycoside antimicrobial drug gentamicin, the rate of resistance in Staphylococcus humanus was lower than in Staphylococcus epidermidis, and the difference was statistically significant ( χ2=11.895, P<0.05); no strains resistant to linezolid and vancomycin were found in both. Comparison of the resistance rates to seven antimicrobial drugs, gentamicin, rifampicin, ciprofloxacin, levofloxacin, moxifloxacin, clindamycin and tetracycline, was significantly higher in MRSA than in MSSA ( χ2=6.169-56.941, P<0.05); however, the resistance rate to cotrimoxazole, MRSA (15.6%, 12/77) was significantly lower than that of MSSA (35.3%, 36/102), and the difference was statistically significant ( χ2=5.155, P<0.05); MRSA and MSSA resistant to linezolid and vancomycin were not found. The resistance rate of Enterococcus faecalis to penicillin G and ampicillin was much higher than that of Enterococcus faecalis, and the difference was statistically significant ( χ2=22.965, P<0.05), and vancomycin-resistant enterococci (VRE) were not found. In conclusion, for staphylococci, except for individual antibiotics, S.hominis and MRSA were more resistant to most antimicrobial drugs than S. epidermidis and MSSA, showing a multidrug-resistant pattern. For enterococci, except for penicillin G and ampicillin resistance rate, Enterococcus faecalis is much higher than Enterococcus faecalis, the rest of the antimicrobial drugs did not see a significant difference, in addition to vancomycin-resistant enterococci were not detected. Clinicians should pay great attention to the monitoring data of multidrug-resistant G +cocci isolated from blood cultures to provide a basis for empirical and rational use of drugs in the clinic, to effectively prevent and reduce the incidence of bloodstream infections caused by G +cocci.

The upset insomnia caused by life and work pressure has seriously affected the physical and mental health of modern people and induced many diseases. The quality of Chinese medicine for nourishing heart and tranquilizing mind is stable, and it has a significant effect on the treatment of insomnia, with fewer adverse reactions, and no dependence on sedative and hypnotic as chemical drugs. The Chinese herbal pieces and preparations for nourishing heart and tranquilizing mind can be divided into psychotropic and sedative drugs according to their functions. Their active ingredients mainly include flavonoids, alkaloids, organic acids, polysaccharides, amino acids and vitamins, etc. They are mostly used in the treatment of cardiovascular diseases and central nervous system inhibition. In this paper, the types and active ingredients and development tendency and application status of the Chinese herbal pieces and preparations of nourishing heart and tranquilizing mind were reviewed individually, in order to provide reference for the development of drugs of nourishing heart and tranquilizing mind in the field of clinical application and related drugs.

Purpose To explore the application and clini-copathological significance of molecular classification in endome-trial cancer(EC)of WHO(2020)tumors of the female repro-ductive system.Methods Sixty-two EC patients were collected and categorized into four subgroups,namely POLE mutation type,mismatch repair deficient(MMRd)type,non-specific molecular spectrum(NMSP)type,and p53 mutation type,based on WHO molecular classification tested by PCR and im-munohistochemistry.The correlation among four molecular sub-groups and their clinicopathological features were analyzed.Re-sults The molecular classification was distributed as follows:3(4.8％)cases were POLE-mutated,15(24.2％)cases MMRd,36(58.1％)cases NSMP and 8(12.9％)cases p53 abnormal expression.There were no significant differences a-mong POLE-mutated and infiltration depth,grade,lymph vascu-lar space invasion and other pathological factors such as lymph node metastasis and FIGO stage(P＞0.05).Among 15 patients with MMRd,the proportion of FIGO stage Ⅱ+Ⅲ significantly increased.One case showed abnormal overexpression of p53 pro-tein,while two cases showed complete loss of expression in MMRd subgroup.36 cases of NSMP were associated with low histopathological grade(Grade Ⅰ+Ⅱ)(P＜0.05),and no significant differences were observed among NSMP and other clinicopathological factors(P＞0.05).The p53 abnormal ex-pression in 8 cases was related to high histopathological grade(Grade Ⅲ)(P＜0.05),and the rate of lymph node metastasis and FIGO stage Ⅱ+Ⅲ significantly increased in patients with p53 abnormal expression,and although the difference was not statistically significant(P＞0.05).Conclusion The molecu-lar subgroups of EC have certain clinical application value,the cases with MMRd and p53 abnormal expression may have poor prognosis than these with POLE-mutated and NSMP.