Congenital blood group chimerism refers to the coexistence of two or more distinct blood types within an individual, resulting from the presence of hematopoietic cell populations with different genotypes. Consequently, red blood cells in such individuals may express different blood group antigens. Based on the timing and mechanism of formation, blood group chimerism can be classified as either congenital or acquired. Although congenital blood group chimerism is rare and involves complex mechanisms, it holds significant implications in transfusion medicine, transplantation, and obstetrics. This article reviews the formation mechanisms, detection methods, and clinical significance of congenital blood group chimerism in transfusion medicine. Particular emphasis is placed on the principles, advantages, and limitations of various detection techniques. Furthermore, the potential applications of these technologies in clinical diagnosis are discussed, providing a technical foundation for the development of precise transfusion strategies.

Tissue repair requires the reconstruction of functional vascular networks to restore oxygen and nutrient delivery, eliminate metabolic waste, and maintain tissue homeostasis. Although biochemical factors such as growth factors and cytokines have been extensively studied in vascular regeneration, increasing evidence indicates that mechanical signals from the extracellular matrix (ECM) are equally important regulators of angiogenesis. Matrix stiffness, as a major biomechanical property of the tissue microenvironment, provides critical information that influences endothelial cell (EC) behavior and vascular remodeling through mechanotransduction. However, the biological effects of matrix stiffness are not universally defined as either pro- or anti-angiogenic, but are highly dependent on tissue context, cellular composition, disease progression, and the dynamic changes occurring during tissue repair. Therefore, understanding how matrix stiffness regulates vascular regeneration is essential for developing more precise strategies for tissue engineering and regenerative medicine. In this review, we summarize recent advances in the regulation of angiogenesis by matrix stiffness during tissue repair from multiple perspectives. First, we discuss the direct effects of matrix stiffness on EC behaviors, including differentiation, morphological remodeling, migration, proliferation, barrier maintenance, and vascular network formation. ECs sense mechanical alterations in the surrounding matrix through various mechanosensitive structures, including integrins, focal adhesion complexes, and mechanosensitive ion channels such as Piezo1 and TRPV proteins. These mechanical signals are subsequently transmitted through intracellular pathways involving FAK, RhoA/ROCK, MAPK, and Hippo-YAP/TAZ signaling, leading to cytoskeletal reorganization and transcriptional regulation. Through these mechanisms, matrix stiffness regulates endothelial functional states and determines the balance between regenerative vascular formation and pathological vascular remodeling. Beyond the direct regulation of ECs, we further highlight the importance of stiffness-mediated intercellular communication within the regenerative microenvironment. Matrix stiffness can regulate the behavior and secretory profiles of vascular-associated cells, including mesenchymal stem cells and macrophages, thereby indirectly affecting endothelial function through paracrine mechanisms. Changes in matrix mechanics influence the secretion of angiogenic factors, inflammatory cytokines, and extracellular vesicles from these cells, creating a mechanical regulation network that coordinates vascular regeneration. This perspective extends the traditional concept of matrix stiffness from a physical support structure to an active regulatory signal that integrates multiple cellular responses during tissue repair. Furthermore, we discuss the tissue-specific effects of matrix stiffness in vascular regeneration across different organs, including the aorta, lung, liver, and heart. Although excessive matrix stiffening is frequently associated with fibrosis and vascular dysfunction, the consequences of mechanical changes vary considerably among tissues. Moderate stiffness alterations may support endothelial activation and vascular stabilization in certain regenerative contexts, whereas persistent pathological stiffening can promote inflammation, endothelial dysfunction, and impaired vascular repair. These findings emphasize that the biological meaning of “soft” and “stiff” microenvironments should be interpreted according to specific tissue and experimental conditions rather than as universal mechanical classifications. Finally, we summarize current challenges and future perspectives in this field. A major limitation is the lack of standardized mechanical characterization among different studies, as stiffness measurements are influenced by material properties, testing methods, and experimental conditions, limiting direct comparison across research systems. Moreover, most existing models fail to fully reproduce the dynamic and viscoelastic properties of native ECM during tissue regeneration. Future studies should combine advanced biomaterials with standardized mechanical analysis, organoid models, and multi-omics approaches to establish more accurate mechanical regulatory maps. Overall, this review proposes that matrix stiffness is not merely a structural feature of tissues, but an active biological signal that regulates vascular regeneration through coordinated mechanotransduction and multicellular interactions. A deeper understanding of stiffness-mediated vascular regulation will provide new theoretical insights and therapeutic opportunities for improving tissue repair outcomes.

ObjectiveTo investigate the protective effect of Astragaloside Ⅳ （AS-Ⅳ） on D-galactose （D-gal）-induced cardiomyocytes senescence and its potential mechanisms. MethodsUsing H9C2 cardiomyocytes as a model， D-gal was used to induce cardiomyocyte senescence. Cell viability was assessed using the CCK-8 assay， senescenceextent was evaluated via β-galactosidase （SA-β-Gal） staining， reactive oxygen species （ROS） levels were measured to assess intracellular oxidative stress， apoptosis extent was determined using the TUNEL assay， and qRT-PCR and Western blot analyses were conducted to examine the expression levels of senescence-related genes and proteins （p21、p53） and key genes （STING， CXCL10， and MX-1） and proteins （STING， cGAS， p-IRF3/IRF3） of the stimulator of interferon genes （STING） pathway. ResultsThe 50 g/L D-gal significantly reduced myocardial cell viability， increased SA-β-Gal positivity， apoptosis rate， and intracellular reactive oxygen species levels， and upregulated the expression of p16， p21， and STING， cGAS， p-IRF3/IRF3 pathway proteins （P< 0.05）； After intervention with 200 μmol/L of AS-Ⅳ， cell viability was significantly enhanced， the SA-β-Gal-positive rate decreased， intracellular reactive oxygen species levels decreased， oxidative stress damage was alleviated， myocardial cell apoptosis was inhibited， and the mRNA and protein levels of aging-related p21 and p53 were downregulated （P＜0.05）. Further detection of STING pathway-related molecules showed that 200 μmol/L of AS-IV inhibited D-galactose-induced STING mRNA and protein expression and reduced p-IRF3/IRF3 protein expression levels， as demonstrated by qRT-PCR and Western blot results. However， the SA-β-Gal positivity rate， intracellular reactive oxygen species （ROS） levels， DNA damage results， and Western blot findings suggested that the STING agonist （STING agonist-7） could reverse the ameliorative effects of AS-Ⅳ on D-galactose-induced cardiomyocytes senescence. ConclusionAS-Ⅳ may mitigate D-gal-induced cardiomyocytes senescence by inhibiting STING pathway activation， providinga new strategy for the prevention and treatment of cardiovascular senescence-related diseases.

Objective:To discuss the changes of adenosine deaminase 2(ADA2)activity in the serum of the systemic lupus erythematosus(SLE)patients,and to clarify its clinical value in the diagnosis and disease assessment of the SLE patients.Methods:According to the inclusion and exclusion criteria,69 SLE patients(SLE group)and 69 healthy controls(control group)were enrolled as study subjects.The disease activity of SLE patients was evaluated by SLE Disease Activity Index(SLEDAI).The ADA2 activity in the serum of the subjects in both groups was detected.The patients were further divided into subgroups based on the presence or absence of the following clinical symptoms:arthritis,myositis,hematuria,proteinuria,pyuria,alopecia,new rash,mucosal ulcer,pleuritis,hypocomplementemia,elevated anti-double-stranded DNA(anti-dsDNA)antibody,thrombocytopenia,and leukopenia.The differences in serum ADA2 activity between joint symptomatic group and joint asymptomatic group were analyzed.The diagnostic efficacy of serum ADA2 activity was evaluated by receiver operating characteristic(ROC)curve analysis.The correlation between ADA2 activity and disease activity in the SLE patients was analyzed by Spearman correlation analysis.Results:Compared with control group,the ADA2 activity in the serum of the patients in SLE group was significantly increased(P<0.01).The ROC analysis results showed that when the cut-off value of ADA2 activity was set at 8.5 U·L-1,the diagnostic performance was optimal,with an area under the curve(AUC)of 0.879(95%CI:0.817-0.940),the specificity was 89.86%,and the sensitivity was 75.36%.The serum ADA2 activity was positively correlated with disease activity in the SLE patients(r=0.32,P=0.007).The subgroup analysis of clinical symptoms results showed that the serum ADA2 activity in the SLE patients with symptoms was significantly higher than that in the SLE patients without symptoms(P<0.01).No significant differences were observed in serum ADA2 activity between the SLE patients with and without myositis,hematuria,proteinuria,pyuria,alopecia,new rash,mucosal ulcer,pleuritis,hypocomplementemia,elevated anti-dsDNA antibody,thrombocytopenia,or leukopenia(P>0.05).Conclusion:The serum ADA2 activity is increased in the SLE patients and can serve as a diagnostic marker for SLE.Serum ADA2 activity is positively correlated with disease activity and is associated with arthritis in the SLE patients,suggesting its potential as an indicator for disease assessment and monitoring.

Poly(lactic-co-glycolide)(PLGA)is a key excipient in long-acting sustained-release preparations,and its degradation properties directly affect the drug release behavior.In this study,PLGA microspheres were prepared by microfluidic techniques,and the morphology changes of the microspheres were observed by scanning electron microscopy(SEM).In alkaline environment,due to the accelerated hydrolysis of ester bonds,the surface of the microspheres was rapidly dissolved and eroded,and the degradation rate was significantly higher than that in acidic environment.High temperature accelerated the degradation of PLGA microspheres.Under neutral and alkaline conditions,the microspheres showed aggregation and adhesion.Under acidic conditions,the microspheres gradually decomposed into irregular fragments.The high ionic strength further promoted the surface corrosion of the microspheres,especially under extreme pH conditions.Simultaneously,PLGA microspheres encapsulating coumarin were prepared to simulate the microsphere formulation.The release rate of coumarin after degradation of the microspheres under different conditions was observed by measuring the absorbance with ultraviolet-visible spectrophotometry.The results were consistent with those of the blank microspheres.This study revealed that the degradation of PLGA microspheres was significantly pH-dependent,temperature sensitive and ion strength responsive.These findings not only helped to understand and optimize the long-term stability and controlled release performance of drug-carrying microspheres,but also provided a theoretical basis for further improvement of PLGA-based drug carrier design.

Microfluidic chips have revolutionized analytical sciences through miniaturization and high-throughput capabilities.However,conventional static devices are constrained by fixed architectures,functional rigidity,and high customization costs.In recent years,,the emerging configurable and reconfigurable microfluidic technologies have provided solutions for these limitations through dynamic adaptability.Configurable systems enable post-fabrication customization via modular assembly or boundary modification,offering cost-effective functional versatility.Reconfigurable microfluidics represents a more advanced paradigm,incorporating real-time decision-making and dynamic control through physical/virtual boundary adjustments during operation.These adaptive systems enable precise manipulation of microenvironments for applications ranging from single-cell manipulation to dynamic biochemical synthesis.In this review,a ″static-dynamic boundary″ framework to systematically analyze both technologies was proposed,and the design rationales,operational mechanisms,and implementation strategies were compared.The development history of these two techniques was introduced,and the applications demonstrated their transformative potential in developing intelligent lab-on-chip systems,while technical challenges in standardization and control interfaces were critically assessed.The development trend on integrating smart materials and AI-driven automation to advance next-generation adaptive microfluidic platforms was prospected.

Forensic medicine has been designated as a first-level discipline,presenting new opportunities and challenges for the development of forensic medicine.Since the 1980s,the establishment of foren-sic medicine discipline and the cultivation of high-level forensic talents have become hot topics in the development of forensic medicine in China.Since the 13th Five-Year Plan,the forensic team of Shanxi Medical University has been aiming at the forefront,proposing the development goals of"Five First-class"and the discipline development path"Six Major Achievements".It has selected benchmark disci-plines,identified gaps in disciplinary development,unified thoughts,formulated completion timelines,concentrated superior resources,assigned tasks to individuals,and created an"Organized Fill-in-the-Blank Format"forensic medicine discipline construction model with the characteristics of the new era.The construction model of forensic medicine has achieved good results in the goals,discipline frame-work,scientific research,talent cultivation,discipline team and platform construction,forming a rela-tively complete discipline construction and management system,and accumulating valuable experience for the construction of first-level discipline and high-level talent cultivation of forensic medicine.

Arginine methylation is a critical post-translational modification that plays multifaceted biological functions. However, the manipulation of protein arginine methylation largely depends on genetic or pharmaceutic inhibition of the regulatory enzymes, protein arginine methyltransferases (PRMTs), or non-methylation substitution of corresponding arginine residue to lysine or alanine of protein of interest (POI), which inevitably affects other substrates, or disrupts the structure of POI. Thus, it urges an approach to specifically modulate the arginine methylation of a POI under physiological conditions. To this end, we report the discovery of a methylation tagging system (MeTAG), that enables targeted modification of protein arginine methylation. Through bridging the methyltransferase PRMT5 proximity to a POI, MeTAG facilitates the arginine methylation of POIs, including known arginine methylated proteins, androgen receptor (AR) and protein kinase B (AKT), as well as a neo-substrate E1A binding protein (p300), in a reversible and PRMT5-dependent manner. Moreover, MeTAG can regulate downstream signaling in a methylation dependent manner, leading to downregulation of PSMA mRNA level and activation of AKT. Therefore, MeTAG represents a feasible approach to modulate protein methylation and thereby perturbs protein function in biological and therapeutic contexts.

Objective To investigate the relationship between the circulating tumor DNA(ctDNA)and the clinicopathological features of epidermal growth factor receptor gene(EGFR),Kirsten rat sarcoma viral oncogene(KRAS),and neuroblastoma RAS viral oncogene(NRAS)in patients with mutant resectable non-small cell lung cancer(NSCLC).Methods Thirty-six patients with NSCLC who underwent surgical resection in our hospital and had matched plasma samples in the biobank were included for mutation analysis.The EGFR,KRAS and NRAS mutations of plasma ctDNA and biopsy tissue were analyzed by peptide nucleic acid clamp PCR to explore the relationship between plasma ctDNA shedding and clinicopathological features of patients.Results The consistency of EGFR,KRAS and NRAS in biopsy tissue and plasma samples of 36 patients was 63.89%(23/36),88.89%(32/36)and 86.11%(31/36),respectively.In mutant tumors,the sensitivity of EGFR,KRAS and NRAS mutation detection in plasma ctDNA was 23.53%(4/17),33.33%(2/6)and 40.00%(2/5),respectively.In patients with adenocarcinoma,plasma ctDNA shedding was associated with higher tumor stage,N stage,TNM stage,tumor necrosis rate,mitotic count 10HPFs,larger maximum tumor diameter and tumor volume(P<0.05).In subgroup analysis of lung adenocarcinoma patients,ctDNA shedding was significantly associated with higher N stage,vascular invasion rate,tumor necrosis rate,and mitotic count 10HPFs,as well as larger maximum tumor diameter and tumor volume(P<0.05).Conclusion The shedding of ctDNA in lung adenocarcinoma is associated with primary tumor diameter,volume,and aggressive histological features(such as necrosis and high mitotic count).

BACKGROUND:Postoperative results with Meek skin grafting in some patients with extremely severe burns have not been satisfactory,with problems of delayed healing or skin graft failure. There have been fewer studies on the treatment of patients with failed Meek skin grafting due to insufficient skin source. This study aimed to explore a treatment method for such patients. OBJECTIVE:To observe the curative effect of stamp-shaped skin allograft in the treatment of severe burns after Meek skin graft failure. METHODS:Twenty-three patients with extremely severe burns who were admitted at Department of Burns and Skin Surgery,the First Affiliated Hospital of the Air Force Medical University from August 2013 to August 2023 with poor healing after Meek skin grafting were enrolled and divided into allogeneic skin treatment group and dressing change group according to different treatment methods. There were 10 cases in the allograft group and 13 cases in the dressing change group. Preoperative hemoglobin,platelet count,albumin count,white blood cell count,neutrophil count,procalcitonin count,and positive rate of microbial culture before secondary Meek skin grafting were compared between two groups. Survival rate of skin grafts before and after the second operation were compared. The number of operations,incidence of sepsis,and wound scars at 3 months and 6 months after operation were retrospectively analyzed. RESULTS AND CONCLUSION:The preoperative hemoglobin,platelet count and albumin count in the allogeneic skin treatment group were significantly higher than those in the dressing change group (Z=-3.172,P=0.002;Z=-3.010,P=0.003;Z=-2.761,P=0.006). There was no significant difference in the preoperative white blood cell count and neutrophil count between the two groups before secondary Meek skin grafting (Z=1.148,P=0.251;Z=0.373,P=0.709),but the serum procalcitonin count in the allogeneic skin treatment group prior to the second operation was significantly lower than that in the dressing change group (Z=2.955,P=0.002). Burn patients in the dressing change group exhibited a higher microbial culture rate than those in the allogeneic skin treatment group (x2=6.303,P=0.029). The survival rate of skin grafts before the second operation in the allogeneic skin treatment group[(74.8±13.3)％]was significantly higher than that in the dressing change group[(58.4±14.2)％;t=2.85,P=0.01). The survival rate of skin grafts after the second stage operation in the allogeneic skin treatment group[(84.0±11.5)％]was significantly higher than that in the dressing change group[(67.6±20.7)％;t=2.24,P=0.03). The frequency of postoperative surgery in the allogeneic skin treatment group was less than that in the dressing change group (Z=2.27,P=0.02). The incidence of sepsis in the dressing change group was significantly higher than that in the allogeneic skin treatment group (x2=5.490,P=0.03). There was no significant difference in the Vancouver Scar Scale scores of the scars between the two groups at 3 and 6 months after operation (t=0.96,1.138,P>0.05). To conclude,stamp-shaped skin allograft has good curative effect in the treatment of wounds with poor healing of skin after Meek micro-transplantation. The utilization rate of skin in the later stage is significantly increased,which reduces the probability of wound infection and solves the problem of insufficient skin source.