This paper systematically reviews the current status of integrated traditional Chinese and western medicine in the treatment of Helicobacter pylori （Hp） infection， as well as recent progress in clinical and basic research both in China and internationally. It summarizes the advantages of traditional Chinese medicine （TCM） in Hp infection management， including improving Hp eradication rates， enhancing antibiotic sensitivity， reducing antimicrobial resistance， decreasing drug-related adverse effects， and ameliorating gastric mucosal lesions. These advantages are particularly evident in patients who are intolerant to bismuth-containing regimens， those with refractory Hp infection， and individuals with precancerous gastric lesions. An integrated， whole-process management approach and individualized， staged comprehensive treatment strategies combining TCM and western medicine are proposed for Hp infection. Future prevention and control of Hp infection should adopt an integrative Chinese-western medical strategy， emphasizing prevention， strengthening primary care， implementing proactive long-term monitoring， optimizing screening strategies， and advancing the development of novel technologies and mechanistic studies of Chinese herbal interventions. These efforts aim to provide a theoretical basis and practical pathways for the establishment and improvement of Hp infection prevention and control systems.

Immobilized enzyme-based enzyme electrode biosensors, characterized by high sensitivity and efficiency, strong specificity, and compact size, demonstrate broad application prospects in life science research, disease diagnosis and monitoring, etc. Immobilization of enzyme is a critical step in determining the performance (stability, sensitivity, and reproducibility) of the biosensors. Random immobilization (physical adsorption, covalent cross-linking, etc.) can easily bring about problems, such as decreased enzyme activity and relatively unstable immobilization. Whereas, directional immobilization utilizing amino acid residue mutation, affinity peptide fusion, or nucleotide-specific binding to restrict the orientation of the enzymes provides new possibilities to solve the problems caused by random immobilization. In this paper, the principles, advantages and disadvantages and the application progress of enzyme electrode biosensors of different directional immobilization strategies for enzyme molecular sensing elements by specific amino acids (lysine, histidine, cysteine, unnatural amino acid) with functional groups introduced based on site-specific mutation, affinity peptides (gold binding peptides, carbon binding peptides, carbohydrate binding domains) fused through genetic engineering, and specific binding between nucleotides and target enzymes (proteins) were reviewed, and the application fields, advantages and limitations of various immobilized enzyme interface characterization techniques were discussed, hoping to provide theoretical and technical guidance for the creation of high-performance enzyme sensing elements and the manufacture of enzyme electrode sensors.

Objective To summarize the clinical and genetic characteristics of end-stage renal disease caused by PLCE1 gene mutations.Methods A retrospective analysis of the clinical and genetic features of three children from a family with PLCE1 gene mutations was conducted,along with a literature review of hereditary kidney disease cases caused by PLCE1 gene mutations.Results The proband was an 8-year-old male presenting with nephrotic syndrome stage 4 chronic kidney disease.Renal biopsy showed focal segmental glomerulosclerosis.Two years and five months after kidney transplantation,the patient had persistent negative proteinuria and normal renal function.Whole-exome sequencing identified two pathogenic heterozygous variants:c.961C>T and c.3255_3256delinsT,with c.3255_3256delinsT being a novel mutation.Family screening revealed no renal involvement in the parents,but among five siblings,one brother died at age of 4 years from end-stage renal disease.A 7-year-old sister presented with proteinuria and bilateral medullary sponge kidney,with proteinuria resolving after one year of follow-up.A 3-year-old brother died after kidney transplantation due to severe pneumonia.The literature review included 45 patients with hereditary kidney disease caused by PLCE1 gene mutations.The main clinical phenotype was nephrotic syndrome(87%,39/45),and renal pathology predominantly showed focal segmental glomerulosclerosis(57%,16/28).No mutation hotspots were identified.Conclusions Compound heterozygous mutations in the PLCE1 gene can lead to rapid progression of the disease to end-stage renal disease,with favorable outcomes following kidney transplantation.Family screening is crucial for early diagnosis,and medullary sponge kidney may be a novel phenotype associated with these gene mutations.Citaion:[Chinese Journal of Contemporary Pediatrics,2025,27(5):580-587]

[Purpose]To analyze the lifetime risk of developing and dying from lung cancer at global and regional levels.[Methods]Data of lung cancer incidence and mortality were obtained from GLOBOCAN 2022 and the population and all-cause mortality data were obtained from the United Nations.The lifetime risk of developing and dying from lung cancer globally and across different regions was estimated by multiple primary adjustment method.[Results]The global lifetime risk of developing lung cancer was 3.59％[95％confidence interval(CI):3.58％～3.59％],ranking third among all cancer types.There were significant gender and regional differences in lifetime risk values.The risk for male was 4.43％(95％CI:4.42％～4.44％),which was higher than that for female(2.71％,95％CI:2.70％～2.72％),with a male-to-female ratio of 1.63.Among regions with varying human development index(HDI)levels,the risk increased with HDI levels,in very high HDI re-gions risk was 5.36％(95％CI:5.34％～5.37％),while in low HDI regions the risk was 0.34％(95％CI:0.33％～0.34％).Among the 20 global regions,East Asia had the highest lifetime risk of 7.53％(95％CI:7.52％～7.55％),while West Africa had the lowest risk of 0.16％(95％CI:0.16％～0.17％).The global lifetime risk of dying from lung cancer was 2.78％(95％CI:2.78％～2.78％),ranking the first among all cancer types.There were significant sex and regional differ-ences in lifetime death risk values.The risk for male was 3.64％(95％CI:3.63％～3.64％),which was higher than that for female(1.89％,95％CI:1.89％～1.90％),with a male-to-female ratio of 1.93.Among regions with varying HDI levels,the risk increased with HDI levels,in very high HDI re-gions the risk was 3.98％(95％CI:3.97％～3.99％),while in low HDI regions the risk was 0.31％(95％CI:0.31％～0.31％).Among the 20 global regions,the Federated States of Micronesia/Poly-nesia had the highest death risk of 5.80％(95％CI:4.98％～6.62％),while West Africa had the lowest risk of 0.15％(95％CI:0.15％～0.16％).The lifetime risk of developing and dying from lung cancer in China was 7.54％(95％CI:7.52％～7.56％)and 5.88％(95％CI:5.87％～5.90％),respec-tively,both ranking the first among all cancer types.[Conclusion]The lifetime risk of developing and dying from lung cancer remains high globally and across different regions,with a particularly heavy burden in high-HDI areas.In China,both the lifetime risk of developing and dying from lung cancer are higher than the global average.This highlights the need for continued enhance-ment of comprehensive prevention and control measures,including addressing lung cancer-related risk factors,as well as improving screening,early diagnosis,and treatment efforts to reduce the lung cancer burden.

Objective:Based on the dataset in the Gene Expression Omnibus database(GEO),we screened out the co-expression modules most relevant to acute myocardial infarction(AMI)and identified ferroptosis-related bio-markers.Methods:We constructed a weighted gene co-expression network for the hypervariable genes in the GSE123342 dataset,screened out the gene modules most related to AMI and identified ferroptosis-related biomark-ers from the key modules,and then observed their expression levels in tissues as well as further analyzed their corre-lation with the immune microenvironment.Results:One key module most relevant to AMI patients was obtained.By intersecting with differential genes,a total of 532 differential genes that were up-regulated in AMI were ob-tained.Functional enrichment analysis showed that they were mainly enriched in biological processes such as granu-locyte migration,reactive oxygen species generation,leukocyte chemotaxis and activation,and defense response regulation.The pathways were mainly enriched in Toll-like signaling pathway,nuclear factor kappa B(NF-κB)signaling pathway,tumor necrosis factor(TNF)signaling pathway,hypoxia-inducible factor-1(HIF-1)signa-ling pathway and cytokine-cytokine receptor interaction pathways,etc.Finally,14 genes were found that were promising targets for AMI treatment:zinc finger antisense 1(ZFAS1),WD repeat domain,phosphoinositide inter-acting 1(WIPI1),Toll-like receptor 4(TLR4),quiescin sulfhydryl oxidase 1(QSOX1),phosphatase and tensin homolog(PTEN),phosphogluconate dehydrogenase(PGD),mitochondrial fusion protein 2(MFN2),double mi-nute 2 homolog(MDM2),mitogen-activated protein kinase 14(MAPK14),mitogen-activated protein kinase 1(MAPK1),gamma-aminobutyric acid receptor-associated protein-like 1(GABARAPL1),arachidonate 5-li-poxygenase(ALOX5),long-chain acyl-CoA synthetase 4(ACSL4),and long-chain acyl-CoA synthetase 1(ACSL1).Correlation analysis revealed that they all had obvious correlations with various immune cells.Conclusion:The 14 ferroptosis genes associated with AMI are expected to become potential immunotherapy targets.

The"capitation payment with retained surplus and shared accountability for reasonable overruns"mechanism constitutes a pivotal institutional framework for advancing the high-quality development of County Medical Communities(CMCs).This study addresses two critical operational challenges:identifying the sources of medical insurance fund surplus and optimizing the governance of fund retention processes.Grounded in transaction cost theory,we develop an analytical framework examining the formation of medical insurance fund surplus through the dual lenses of intra-organizational dynamics within CMCs and external medical insurance payment mechanism design.Utilizing Deqing County,Zhejiang Province as an empirical case,this research proposes a five-pronged strategy:Clarifying generation channels of insurance fund surplus,scientifically determining regional medical insurance budgets,implementing bundled payment mechanisms for CMCs,adopting hybrid payment models integrating unified and differentiated approaches,and establishing performance-based incentive systems.These findings elucidate the formative pathways of medical insurance fund surplus while offering theoretical and practical insights for enhancing payment system reforms to support CMC development.

This study evaluated the potential of OPC-167832 as a new method for the treatment of Mycobacterium fortuitum infec-tion.Drug sensitivity tests were conducted with the broth microdilution method to determine the minimum inhibitory concentration(MIC)of OPC-167832 against standard strains of M.fortuitum and 44 clinical isolates of M.fortuitum.A DprE1 overexpression strain was constructed,and the effect in the MIC of OPC-167832 against M.fortuitum were explored.Intracellular germicidal tests and checkerboard tests were conducted to verify the ability of OPC-167832 to kill intracellular M.fortuitum,and its interaction with five drugs:amikacin,clarithromycin,imipenem,moxifloxacin,and clofazimine.The MIC50 and MIC90 against 44 clinical isolates of M.fortuitum were 0.031 25 μg/mL and 0.062 5μg/mL,respectively.The epidemiological cut-off value(ECOFF)was 0.062 5 μg/mL.Overexpression of DprE1 led to resistance to OPC-167832 in M.fortuitum.After 24 hours of incubation,the intracellular bacterial in-hibition rate of OPC-167832 at a 1 μg/mL concentration was 81.37%,exceeding the 74.05%inhibition rate of amikacin at a 1 μg/mL concentration.OPC-167832 showed strong inhibitory activity against M.fortuitum in vitro and in macrophages,and might provide a promising treatment for M.fortuitum infection.

Depression,characterized by high incidence,high re-lapse rate and high suicide rate,is an affective disorder mainly characterized by low mood and often accompanied by suicidal tendency,which seriously endangers human health.In recent years,more and more evidence suggests that microglia regulate synaptic plasticity and play an important role in depression.Here we outline the recent research progress of microglia regula-ting synaptic plasticity to exert antidepressant effects,focusing on three main types of molecular signals regulating synaptic pruning in microglia,including"Find Me"signaling,"Eat Me"signaling and"Don't Eat Me"signaling.By reviewing recent studies on how microglia regulate synaptic plasticity in depression,hopeful-ly,the understanding of microglia-mediated synaptic plasticity can be strengthened,which can help to provide new strategies for the treatment of depression by targeting microglia or microglia-associated signaling pathways.

Aim To explore the protective effect of the isochroman compound Asperisochroman B(AB)on oxygen-glucose deprivation/reoxygenation(OGD/R)injury of neurons based on the PI3K/AKT/Foxo1 path-way and to reveal the related mechanism.Methods Primary neurons were cultured and the OGD/R model was constructed.The primary neurons were divided in-to the blank control group,OGD/R group,and AB low,medium,and high concentration(3,10,30 μmol·L-1)groups.The effects of AB on primary neurons were determined by CCK-8 assay,lactate dehydrogen-ase(LDH)release assay,and Hoechst 33342 stai-ning.The expression levels of PI3K,AKT,and Foxo1-related proteins were detected by Western blot.After intervention with the PI3K inhibitor(LY294002)and re-modeling and intervention with high concentra-tion of AB(30 μmol·L-1),the expression of PI3K/Foxo1 pathway-related proteins was detected by West-ern blot.Results Compared with the OGD/R group,AB could significantly increase the cell survival rate of primary neurons and reduce the release of LDH.The results of Hoechst 33342 and immunofluorescence stai-ning showed that AB reduced apoptosis after OGD/R injury.Western blot results showed that compared with the OGD/R group,after AB intervention,the expres-sion levels of Bcl-2 and NeuN proteins in neurons sig-nificantly increased(P＜0.01),and the expression level of Bax protein significantly decreased(P＜0.01).At the same time,it upregulated the expres-sion levels of p-AKT and PI3K proteins,promoted Foxo1 phosphorylation,and downregulated the expres-sion of Foxo1.Compared with the high-dose AB group,LY294002 could inhibit the changes of the a-bove indicators and reverse the protective effect of AB on OGD/R-injured primary neurons.Conclusions AB can alleviate oxygen-glucose deprivation/reoxygen-ation-induced neuronal injury,and its mechanism may be related to the activation of the PI3K/AKT/Foxo1 signaling pathway.

Scholarly articles published in the Web of Science database from January 1,2004 to November 10,2024 in the field of medical device utilization management were collected.CiteSpace-based bibliometric analysis of the included literature was performed in terms of the year of publication,region of publication,highly cited literature and highly cited journals and keywords.The Internet of Things(IoT),cloud computing and wearable devices were identified as the current research hotspots in the field of medical device utilization management.References were provided for further research related to medical device utilization management.[Chinese Medical Equipment Journal,2025,46(7):63-67]