Objective: To accurately determine ABO blood groups through serological and molecular biological tests in patients whose forward typing was group O but who showed weak antibodies on one side of reverse typing, thereby ensuring precise transfusion. Methods: A total of 160 cases from 2023 to 2025 at Tianjin Blood Center, initially screened as O type with weak antibodies or missing antibodies on one side of reverse typing, were collected. Serological tests absorption-elution tests, and molecular biological tests were performed to accurately identify their ABO blood groups and ensure transfusion safety. Results: Among the 160 patients with forward typing as O type and weak antibodies on one side of reverse typing, 92 were identified as O type, 46 as ABO subtypes already named and recorded by ISBT (mainly including 18 cases of Ael02, 8 cases of AW37, and 9 cases of Bel03), 12 suspected as new alleles not yet recorded by ISBT (among which 5 were suspected to carry novel alleles that have not been recorded or reported in the literature), and 10 were suspected as weakened A/B antigens. Conclusion: In clinical transfusion, attention should be paid to cases with ABO forward-reverse discrepancy, where forward typing is O type and reverse typing shows weak antibodies on one side. These cases may involve ABO subtypes, and further testin is necessary to accurately determine the ABO blood group, achieve precise transfusion, and avoid blood wastage.

Objective:To investigate the expression and methylation status of the SALL4 gene in placental tissues of fetal growth restriction (FGR) and its effects on trophoblast cell proliferation, migration, and invasion. Methods:Placental tissues were collected from 20 full-term FGR patients and 20 healthy term controls who underwent regular prenatal examination and cesarean section at the Third Affiliated Hospital, Zhengzhou University between July 2023 and February 2024. SALL4 mRNA and protein expression were analyzed by quantitative real-time polymerase chain reaction (qRT-PCR) and Western blot. Methylation specific polymerase china reaction (MSP) assessed promoter methylation levels. HTR8/SVneo cells were transfected with SALL4-targeting small interfering RNA (si-SALL4) or negative control small interfering RNA (si-NC). HTR8/SVneo cells were treated with the demethylating agent 5-aza-2′-deoxycytidine (5-Aza-dC) to inhibit gene methylation (5-Aza-dC group) or with 10% RPMI-1640 medium as a vehicle control. Transfection efficiency (for siRNA) and the efficacy of 5-Aza-dC-induced demethylation were assessed by qRT-PCR and Western blot. The functional effects of SALL4 knockdown and methylation inhibition on trophoblast cells were evaluated using proliferation assays, scratch wound healing assays, and Transwell invasion assays. Statistical analyses included independent t-tests and Chi-square test. Results:(1) Human tissues: FGR placentas showed lower SALL4 mRNA (0.802±0.194 vs. 1.015±0.186, t=3.55) and protein expression (0.445±0.114 vs. 0.701±0.113, t=3.19), alongside higher methylation rates of SALL4 [80% (16/20) vs. 15% (3/20), χ2=14.44] compared to controls (all P<0.05). (2) In vitro: si-SALL4 transfection reduced HTR8/SVneo proliferation (OD450 at 48 h: 0.653±0.021 vs. 0.827±0.040, t=6.60), migration [healing rate at 48 h: (24.317±2.637)% vs. (49.327±1.961)%, t=13.18], and invasion [counted invaded cells: (133.000±6.557) vs. (272.667±18.009) cells, t=12.62] versus si-NC (all P<0.05). Conversely, 5-Aza-dC treatment increased HTR8/SVneo proliferation (0.917±0.042 vs. 0.783±0.031, t=－4.47), migration [(71.097±3.354)% vs. (51.632±2.877)%, t=－7.63], and invasion [(384.000±12.166) vs. (202.833±7.095) cells, t=－13.69] versus vehicle control (all P<0.05). Conclusions:Hypermethylation of the SALL4 promoter in FGR placentas suppresses its expression, impairing trophoblast cell function. Demethylation restores SALL4 expression and enhances cellular proliferation, migration, and invasion, involving in the occurrence and development of FGR disease.

[Objective]To investigates the pathogenesis and clinical management of airway remodeling in chronic obstructive pulmonary disease(COPD)through the lens of mitochondrial functionality,based on the theoretical framework of"Xuanfu".[Methods]Through review of modern literature and classical Chinese medical ancient books it explores the link between mitochondrial dysfunction and COPD airway remodeling,examines how the"Xuanfu"theory relates to mitochondrial function in both physiological and pathological contexts,discusses the traditional Chinese medical(TCM)pathogenesis of COPD airway remodeling,summarizes treatment principles,and highlights contemporary studies supporting the role of TCM in modulating mitochondrial function.[Results]Mitochondrial dysfunction is crucial in COPD airway remodeling,with mechanisms and clinical manifestations aligning with"Xuanfu obstruction"and"lung collateral damage"in TCM.Based on the"Xuanfu"theory,the core pathogenesis can be described as"Xuanfu obstruction,lung collateral damage".The treatment should focus on utilizing pungent agents to disperse and ventilate,regulating Qi to open Xuanfu portals,expelling phlegm and resolving static blood,alleviating depression to free collateral vessels,reinforcing healthy Qi while eliminating pathogenic factors,strategically harmonizing unblocking with tonifying interventions.Contemporary studies indicate that intervention with traditional Chinese herbal formulas may repair pulmonary tissue damage and inhibit airway remodeling.These effects are mediated through mechanisms including the enhancement of mitochondrial energy metabolism and the promotion of mitophagy and mitochondrial biogenesis.These findings provide a modern scientific basis for the traditional pathogenesis of"Xuanfu obstruction,lung collateral damage"and its corresponding therapeutic principles in TCM.[Conclusion]The thesis propose mitochondrial dysfunction as the key pathophysiological link between the TCM mechanism of"Xuanfu obstruction,lung collateral damage"and airway remodeling in COPD.This framework establishes mitochondrial homeostasis as a core therapeutic target for TCM interventions,offering a novel basis for integrating traditional theory with modern cellular mechanisms in COPD diagnosis and treatment.

Parkinson's disease (PD) is a neurodegenerative disorder characterized by the progressive loss of dopaminergic neurons and the accumulation of Lewy bodies, leading to motor and nonmotor symptoms. While both genetic and environmental factors contribute to PD, recent studies highlight the crucial role of lipid metabolism disturbances in disease progression. Altered lipid homeostasis promotes protein aggregation and oxidative stress, with significant changes in lipid classes such as sphingolipids and glycerolipids observed in patients with PD. These disturbances are involved in key pathological processes, such as α-synuclein aggregation, organelle dysfunction, lipid-mediated neuroinflammation, and impaired lipid homeostasis. This review examines the relationship between lipid species and PD progression, focusing on the physiological roles of lipids in the central nervous system. It explores the mechanistic links between lipid metabolism and PD pathology, along with lipid-related genetic risk factors. Furthermore, this review discusses lipid-targeting therapeutic strategies to mitigate PD progression, emphasizing the potential of lipid modulation for effective treatment development.
Humans ; Parkinson Disease/metabolism* ; Lipid Metabolism/physiology* ; Animals ; Oxidative Stress/physiology* ; alpha-Synuclein/metabolism*

Objective To extract the core elements and connotation definitions of the concept of organizational resilience of County Medical Community (CMC),in order to explore effective ways to enhance the organizational resilience of CMC.Methods Based on the Atomic spectrum,as of October 31,2023,52 articles related to organizational resilience in the health system were included for concept images extraction,calculating the frequency and occurrence rate of concept images,extracting the concept of organizational resilience in the health system,and deducing the core elements and definitions of the concept of organizational resilience in CMC were derived through the comparison of similarities and differences.Results Although both the healthcare system and the CMC are composite organizations,there are differences in environmental pressure,organizational size,and resource reserves.The concept of organizational resilience of CMC is defined as the advanced process of resilience functions exhibited by CMC in response to emergencies,internal and external threats,and social pressures that constrain the sustainable development of the organization,including redundant preparation,stable recovery,and response to growth,as well as their ability to absorb,adapt,and transform disruptive events.This not only maintains the basic structure and functions of the organization,but also enables the organization to grow against the trend.Conclusion Breaking through the traditional hierarchical structure in terms of structural resilience,achieving a deep integration and coordination mechanism of the medical community horizontally and vertically.Breaking through traditional static planar functions in terms of functional resilience,enhancing the driving force within the medical community through dynamic growth mechanisms.

Objective To extract the core elements and connotation definitions of the concept of organizational resilience of County Medical Community (CMC),in order to explore effective ways to enhance the organizational resilience of CMC.Methods Based on the Atomic spectrum,as of October 31,2023,52 articles related to organizational resilience in the health system were included for concept images extraction,calculating the frequency and occurrence rate of concept images,extracting the concept of organizational resilience in the health system,and deducing the core elements and definitions of the concept of organizational resilience in CMC were derived through the comparison of similarities and differences.Results Although both the healthcare system and the CMC are composite organizations,there are differences in environmental pressure,organizational size,and resource reserves.The concept of organizational resilience of CMC is defined as the advanced process of resilience functions exhibited by CMC in response to emergencies,internal and external threats,and social pressures that constrain the sustainable development of the organization,including redundant preparation,stable recovery,and response to growth,as well as their ability to absorb,adapt,and transform disruptive events.This not only maintains the basic structure and functions of the organization,but also enables the organization to grow against the trend.Conclusion Breaking through the traditional hierarchical structure in terms of structural resilience,achieving a deep integration and coordination mechanism of the medical community horizontally and vertically.Breaking through traditional static planar functions in terms of functional resilience,enhancing the driving force within the medical community through dynamic growth mechanisms.

[Objective]To investigates the pathogenesis and clinical management of airway remodeling in chronic obstructive pulmonary disease(COPD)through the lens of mitochondrial functionality,based on the theoretical framework of"Xuanfu".[Methods]Through review of modern literature and classical Chinese medical ancient books it explores the link between mitochondrial dysfunction and COPD airway remodeling,examines how the"Xuanfu"theory relates to mitochondrial function in both physiological and pathological contexts,discusses the traditional Chinese medical(TCM)pathogenesis of COPD airway remodeling,summarizes treatment principles,and highlights contemporary studies supporting the role of TCM in modulating mitochondrial function.[Results]Mitochondrial dysfunction is crucial in COPD airway remodeling,with mechanisms and clinical manifestations aligning with"Xuanfu obstruction"and"lung collateral damage"in TCM.Based on the"Xuanfu"theory,the core pathogenesis can be described as"Xuanfu obstruction,lung collateral damage".The treatment should focus on utilizing pungent agents to disperse and ventilate,regulating Qi to open Xuanfu portals,expelling phlegm and resolving static blood,alleviating depression to free collateral vessels,reinforcing healthy Qi while eliminating pathogenic factors,strategically harmonizing unblocking with tonifying interventions.Contemporary studies indicate that intervention with traditional Chinese herbal formulas may repair pulmonary tissue damage and inhibit airway remodeling.These effects are mediated through mechanisms including the enhancement of mitochondrial energy metabolism and the promotion of mitophagy and mitochondrial biogenesis.These findings provide a modern scientific basis for the traditional pathogenesis of"Xuanfu obstruction,lung collateral damage"and its corresponding therapeutic principles in TCM.[Conclusion]The thesis propose mitochondrial dysfunction as the key pathophysiological link between the TCM mechanism of"Xuanfu obstruction,lung collateral damage"and airway remodeling in COPD.This framework establishes mitochondrial homeostasis as a core therapeutic target for TCM interventions,offering a novel basis for integrating traditional theory with modern cellular mechanisms in COPD diagnosis and treatment.

Objective:To investigate the expression and methylation status of the SALL4 gene in placental tissues of fetal growth restriction (FGR) and its effects on trophoblast cell proliferation, migration, and invasion. Methods:Placental tissues were collected from 20 full-term FGR patients and 20 healthy term controls who underwent regular prenatal examination and cesarean section at the Third Affiliated Hospital, Zhengzhou University between July 2023 and February 2024. SALL4 mRNA and protein expression were analyzed by quantitative real-time polymerase chain reaction (qRT-PCR) and Western blot. Methylation specific polymerase china reaction (MSP) assessed promoter methylation levels. HTR8/SVneo cells were transfected with SALL4-targeting small interfering RNA (si-SALL4) or negative control small interfering RNA (si-NC). HTR8/SVneo cells were treated with the demethylating agent 5-aza-2′-deoxycytidine (5-Aza-dC) to inhibit gene methylation (5-Aza-dC group) or with 10% RPMI-1640 medium as a vehicle control. Transfection efficiency (for siRNA) and the efficacy of 5-Aza-dC-induced demethylation were assessed by qRT-PCR and Western blot. The functional effects of SALL4 knockdown and methylation inhibition on trophoblast cells were evaluated using proliferation assays, scratch wound healing assays, and Transwell invasion assays. Statistical analyses included independent t-tests and Chi-square test. Results:(1) Human tissues: FGR placentas showed lower SALL4 mRNA (0.802±0.194 vs. 1.015±0.186, t=3.55) and protein expression (0.445±0.114 vs. 0.701±0.113, t=3.19), alongside higher methylation rates of SALL4 [80% (16/20) vs. 15% (3/20), χ2=14.44] compared to controls (all P<0.05). (2) In vitro: si-SALL4 transfection reduced HTR8/SVneo proliferation (OD450 at 48 h: 0.653±0.021 vs. 0.827±0.040, t=6.60), migration [healing rate at 48 h: (24.317±2.637)% vs. (49.327±1.961)%, t=13.18], and invasion [counted invaded cells: (133.000±6.557) vs. (272.667±18.009) cells, t=12.62] versus si-NC (all P<0.05). Conversely, 5-Aza-dC treatment increased HTR8/SVneo proliferation (0.917±0.042 vs. 0.783±0.031, t=－4.47), migration [(71.097±3.354)% vs. (51.632±2.877)%, t=－7.63], and invasion [(384.000±12.166) vs. (202.833±7.095) cells, t=－13.69] versus vehicle control (all P<0.05). Conclusions:Hypermethylation of the SALL4 promoter in FGR placentas suppresses its expression, impairing trophoblast cell function. Demethylation restores SALL4 expression and enhances cellular proliferation, migration, and invasion, involving in the occurrence and development of FGR disease.

Objective To investigate the serological and molecular characteristics of twenty blood samples carrying ABO?AW.37 allele and to analyze ABO allelic enhancement.Methods The ABO phenotype of the twenty samples was de-termined by serological methods and the genotype of 1-7 ABO exons was analyzed by Sanger sequencing.Results Sequen-cing analysis showed that all twenty samples contained a c.940A>G(p.Lys314Glu)mutation of A allele,which was defined as ABO?AW.37.When ABO?AW.37 and B alleles were inherited simultaneously in 9 cases,in forward typing anti-A anti-bodies all agglutinated and the serological phenotype was Aw B.Among the 11 cases with ABO?AW.37 and O alleles inherited simultaneously,there was no agglutination of anti-A in forward typing.For absorption and elution tests,5 cases were weakly positive and the serological phenotype was Ael,while 6 cases were negative for absorption and elution tests and the serologi-cal phenotype was O type.Conclusion Allelic enhancement occured when both ABO?AW.37 allele and B allele were in-herited simultaneously.When ABO? AW.37 was inherited simultaneously with O allele,the serological phenotype was Aelor O type and attention should be paid to blood type identification.

Objective·To identify the functional motifs of mucin 1(MUC1)involved in regulating tumor cell proliferation,migration,and stemness maintenance.Methods·Mutational characteristics of the MUC1 gene across different cancers were identified from The Cancer Genome Atlas(TCGA)database.Various MUC1 mutation sites were analyzed and localized,followed by ranking based on mutation frequency.Western blotting was used to screen high-frequency MUC1 mutants with stable protein expression.BT549 cell line with MUC1 knocked out and MCF-10A cell line were used to stably overexpress MUC1 wild-type(MUC1-WT)and mutants by using lentiviral technology.Immunofluorescence was used to detect the cellular localization of MUC1 mutants.Using MUC1-WT as a positive control and MUC1-AQA,a loss-of-function mutant,as a negative control,the biological functions of different MUC1 mutant cells were analyzed:cell proliferation ability was assessed by cell counting kit-8(CCK-8)assay and colony formation assay;cell migration ability was evaluated by wound-healing and Transwell assays;cell stemness was examined by sphere formation assay.Structural localization of MUC1 mutants was analyzed by using PyMOL software,and molecular docking analysis was performed by using a protein docking software(ZDOCK Server).Results·A total of 102 mutations located in the MUC1 coding region were identified in the TCGA database,among which five missense mutations(P418S,S251R,V359I,N271S,and N465H)exhibited higher frequencies and were located in the non-variable number of tandem repeats(non-VNTR)region.Further examination revealed that the MUC1-S251R,N271S,and V359I mutants could be stably expressed.The cellular localization assay indicated that these three mutants predominantly localized in the cytoplasm,but were also presented in the nucleus.The nuclear-to-cytoplasmic ratio showed minimal differences between MUC1-WT and the mutants.Analysis of the tumorigenic biological functions of the cells expressing different MUC1 mutants revealed that:① High expression of MUC1-WT significantly enhanced the proliferation ability of both BT549 and MCF-10A cells;the proliferation of MUC1-AQA,S251R,and N271S mutant cells was decreased compared to MUC1-WT cells,while MUC1-V359I mutant cells exhibited a similar proliferative profile to MUC1-WT cells.② The migration ability of MUC1-WT high-expressing cells was significantly enhanced,whereas MUC1-AQA cells demonstrated attenuated migration.In the BT549 cells,the migration ability of MUC1-S251R and V359I cells was similar to that of MUC1-WT cells,whereas MUC1-N271S cells showed reduced migration.In the MCF-10A cells,the migration ability of MUC1-N271S and MUC1-V359I cells was similar to that of MUC1-WT cells,whereas MUC1-S251R cells exhibited significantly decreased migration.③ Stemness was enhanced in both cell types with high MUC1-WT expression,while MUC1-AQA cells lost stemness;the cells with MUC1-N271S,V359I and MUC1-WT showed comparable maintenance of stemness,whereas MUC1-S251R cells demonstrated compromised stemness.PyMOL software analysis unveiled that MUC1-N271S and V359I were located in or around the sperm protein-enterokinase-agarin(SEA)region,specifically in the loop region and the β-sheet,respectively.The molecular docking analysis revealed that the stability of the complex formed by MUC1-WT or V359I with the extracellular domain of epidermal growth factor receptor(EGFR)surpassed that of MUC1-N271S or S251R,indicating a stability hierarchy of V359I>WT>N271S>S251R.Conclusion·MUC1 mutants exhibit diverse impacts on the biological functions of tumor cells,with their effects on proliferation correlating with the EGFR signaling pathway.MUC1-V359I is similar to MUC1-WT,indicating a negligible effect on tumor cell proliferation,migration,and stemness maintenance.Conversely,MUC1-S251 and N271 sites may be involved in the regulation of signaling pathways governing cell proliferation and migration and the MUC1-S251 site plays a critical role in maintaining cell stemness.