Biomedical subjects

Jiajun Zhang

Publications and source records attributed to Jiajun Zhang.

3 recordsLinked to original sources

PubMed2026

Concurrence of antibiotic resistance genes in plasmid genomes shape environmental resistomes.

Horizontal transfer of plasmid-associated antibiotic resistance genes (ARGs) plays a pivotal role in environmental antibiotic resistance dissemination. Here, we characterized ARG concurrence patterns in plasmid genomes and examined plasmid-associated ARGs across 106 environmental metagenomes. Approximately half of known ARG subtypes (257) occurred in plasmid genomes, and nearly one-quarter of plasmids carried ARGs, including "super plasmids" harboring over 20 ARG subtypes spanning 10 antibiotic categories. Aminoglycoside resistance genes (AmRGs) exhibited the highest concurrence frequency (CF) with other ARGs in plasmid genomes, followed by beta-lactam and sulfonamide resistance genes. Many high-risk ARGs preferentially coexisted with AmRGs (45.6% of total AmRGs CF). Environmental metagenomes revealed distinct plasmid-associated ARG profiles between polluted and relatively pristine environments, with significantly greater diversity and abundance under anthropogenic pollution. Five widespread ARG subtypes occurred across all environmental media, whereas polluted environments contained more unique ARGs. Co-occurrence networks identified AmRGs as "hubs" linking multiple ARG subtypes in environmental resistomes. Plasmid-ARG interaction networks further showed more complex potential plasmid-mediated concurrent dissemination in polluted environments. Collectively, use of aminoglycosides is more likely to cause co-transmission of multiple plasmid-related ARGs than other antibiotics, and CF of ARGs is proposed as an important supplementary factor for evaluating ARG dissemination under anthropogenic antibiotic stress.

Antibiotic resistance genes (ARGs)↗

PubMed2026

Influence of FAM13A gene polymorphism and serum matrix metalloproteinases 9 and 12 on the phenotypes of chronic obstructive pulmonary disease.

PURPOSE: FAM13A as a susceptibility gene for chronic obstructive pulmonary disease(COPD).Many studies verified that FAM13A involved epithelial‒mesenchymal transition (EMT) via the TGF-β1 pathway, some accompanied by an increase in MMP levels. The present study aimed to explore the disease susceptibility of the FAM13A gene, with clinical phenotypes, and investigate the relationships between FAM13A SNP loci and the serum levels of MMP-9 and MMP-12. PATIENTS AND METHODS: We recurited 497 patients with stable COPD patients and 303 healthy controls. Data on blood tests, pulmonary function, and HRCT imaging were collected. Serum MMP-9 and MMP-12 levels were measured by ELISA. Genomic DNA was extracted, and SNPs in the FAM13A gene were detected using targeted region genotyping chips. Logistic regression analysis was performed to assess the associations between SNP loci and COPD susceptibility. Differences in pulmonary function, haematological indicators, bronchial wall thickness, and emphysema parameters among different genotypes were evaluated. Multiple linear regression analysis was used to explore the relationship between genotypes and serum MMP-12 level. RESULTS: We screened a total of 476 SNPs and identified the rs2869947 polymorphism in the FAM13A gene as significantly associated with an increased risk of COPD,Stratified analyses further revealed that this association was particularly in males and individual with BMI ≥ 24.Serum levels of MMP-9 and MMP-12 were significantly higher in COPD patients compared with healthy controls. Genotype(AA vs.GG) showed no significant association with pulmonary function severity,bronchial wall indices,hematological marker,and serum MMP-9 levels in COPD patients(P > 0.05).Compared with GG genotype, AA genotype presented significantly higher LAA-950% and serum MMP-12 levels (P = 0.049 and P = 0.023). CONCLUSION: Our findings suggest that the FAM13A SNP rs2869947 may be associated with COPD susceptibility in the Han Chinese population. The FAM13A AA genotype increased serum MMP-12 levels and correlated with emphysema phenotype.

Humans↗

PubMed2025

Barrier effects on the kinetics of cohesin-mediated loop extrusion.

Chromosome organization mediated by structural maintenance of chromosome complexes is crucial in many organisms. Cohesin extrudes chromatin into loops that are thought to lengthen until it is obstructed by CTCF proteins. In complex cellular environments, the loop extrusion machinery may encounter other chromatin-binding proteins. How these proteins interfere with the cohesin-meditated extrusion process is largely unexplored, but recent experiments have shown that some proteins serve as physical barriers that block cohesin translocation. Other proteins containing a cohesin-interaction motif serve as chemical barriers to induce cohesin pausing through interactions with it. Here, we develop an analytically solvable approach for the loop extrusion model incorporating barriers to investigate the effect of the barrier on the passive extrusion process. To further quantify the impact of barriers, we calculate the mean looping time it takes for cohesin to translocate to form a stable loop before dissociation. Our finding reveals that the physical barrier can accelerate the loop formation, and the degree of acceleration is closely related to the impedance strength of the physical barrier. In particular, the synergy of the cohesin loading site and the physical barrier site accelerates loop formation more significantly. The proximity of the cohesin loading site to the barrier site facilitates the rapid formation of stable loops in long genomes, which implies loop extrusion and chromatin-binding proteins might shape functional genomic organization. Conversely, chemical barriers consistently impede loop formation, with increasing impedance strength of the chemical barrier leading to longer loop formation time. Our study contributes to a more comprehensive understanding of the complexity of the loop extrusion process, providing a new perspective on the potential mechanisms of gene regulation.

Cohesins↗