Biomedical subjects

Wei Yu

Publications and source records attributed to Wei Yu.

3 recordsLinked to original sources

PubMed2026

Surgical outcomes and complications of fixation strategies for distal tibial fractures: a systematic review and network meta-analysis.

BACKGROUND: Multiple fixation options exist for distal tibial fractures, but the optimal approach remains controversial. Common techniques includeopen reduction and internal fixation(ORIF), minimally invasive plate osteosynthesis (MIPO), external fixation combined with limited open reduction and internal fixation (EF + LORIF), intramedullary nailing (IMN), and retrograde tibial nailing (RTN). METHODS: PubMed, Embase, Web of Science, and the Cochrane Library were searched through March 19, 2026. Network meta-analysis (R v4.5.1) assessed operation time, fracture healing time, malunion, delayed union/nonunion, and infection, reporting MDs or RRs with 95% CIs. RESULTS: Eleven randomized controlled trials and 18 cohort studies (2145 patients) were included. MIPO was associated with a longer operative time and a longer time to union than IMN-IP (MD = 8.23, 95% CI 0.44-16.01; and MD = 1.02, 95% CI 0.10-1.93, respectively). For malunion, ORIF had a lower risk than MIPO (RR = 0.30, 95% CI 0.11-0.82), whereas MIPO had a higher risk than EF + LORIF (RR = 3.26, 95% CI 1.08-9.80) and IMN-SP (RR = 4.03, 95% CI 1.30-12.48). ORIF, EF + LORIF, and IMN-SP also showed lower malunion risk than IMN-IP. No significant differences were observed for delayed union and nonunion. Infection risk was generally higher with ORIF and MIPO than with several comparators, particularly EF + LORIF and intramedullary nailing-based strategies. CONCLUSIONS: No single strategy was consistently superior. Operation time and impaired union ( delayed union and nonunion) did not differ significantly among techniques. MIPO may be associated with longer time to union than IMN-IP and higher malunion risk than EF + LORIF and IMN-SP. Infection risk appeared higher with ORIF and MIPO in network estimates, although several comparisons remained uncertain. Findings should be interpreted in light of imprecision and study-level heterogeneity. PROTOCOL REGISTRATION: INPLASY2025120055.

Humans↗

PubMed2026

Molecular epidemiology of levofloxacin-resistant Klebsiella pneumoniae and the association of plasmid-mediated quinolone resistance genes with key biological phenotypes.

UNLABELLED: Klebsiella pneumoniae is a major opportunistic pathogen in China, yet the molecular epidemiology of quinolone resistance remains poorly characterized. This study analyzed 2,433 clinical isolates from 37 Chinese hospitals (2018-2022). The overall levofloxacin-non-susceptible (NS) rate was 53.60%, with urinary tract isolates showing higher resistance. Whole-genome sequencing identified 12 plasmid-mediated quinolone resistance (PMQR) genes. Among 1,304 NS strains, 74.54% carried at least one PMQR gene (mainly qnrS, qnrB, and aac(6')-Ib-cr), and 60.20% also had quinolone resistance-determining region (QRDR) mutations. Functional studies revealed diverse phenotypic impacts. Most PMQR genes conferred low-level resistance (minimum inhibitory concentration [MIC] = 1 mg/L), while qnrB52 and qnrB91 caused high-level resistance (MIC = 8-16 mg/L). Notably, qnrB91 reduced biofilm formation, indicating a trade-off between resistance and colonization. Growth assays showed that qnrB52, qnrB91, and qnrS1 inhibited normal growth, whereas qepA1 and qnrS1 enhanced growth under ethanol stress. Most PMQR genes (except qnrB6) attenuated bacterial adhesion. qepA1 promoted intracellular survival in macrophages, suggesting a role in chronic infection. Animal models confirmed that qnrB6, qnrB7, qnrVC6, and aac(6')-Ib-cr significantly enhanced virulence. This study is the first in China to report qnrVC6 and novel gyrA mutations (Ser83Ala/Val, Asp87Phe/His) in K. pneumoniae. It systematically reveals how PMQR genes influence infection by modulating resistance, immune evasion, and pathogenicity. These findings highlight that PMQR genes contribute not only to antibiotic resistance but also to virulence, suggesting that treatment strategies should consider specific PMQR genotypes. This research provides the largest-scale molecular epidemiological data and a theoretical basis for controlling quinolone-resistant K. pneumoniae in China. IMPORTANCE: Quinolone-resistant Klebsiella pneumoniae poses a serious threat to public health, yet the role of plasmid-mediated quinolone resistance (PMQR) genes beyond antibiotic resistance remains underexplored. In this largest-scale multicenter study in China, we analyzed 2,433 clinical isolates and discovered that PMQR genes do more than just confer drug resistance-they also influence bacterial growth, stress survival, biofilm formation, and the ability to evade or persist within host immune cells. Some PMQR genes even enhance virulence in an animal model. These findings challenge the traditional view of resistance genes as mere contributors to drug failure, revealing that they can also shape infection outcomes by altering bacterial behavior. Understanding these dual roles may guide more precise treatment strategies targeting specific PMQR genotypes.

Klebsiella pneumoniae↗

PubMed2025

YAP/TEAD4/SP1-induced VISTA expression as a tumor cell-intrinsic mechanism of immunosuppression in colorectal cancer.

Hyperactivation of the YAP/TEAD transcriptional complex in cancers facilitates the development of an immunosuppressive tumor microenvironment. Herein, we observed that the transcription factor SP1 physically interacts with and stabilizes the YAP/TEAD complex at regulatory genomic loci in colorectal cancer (CRC). In response to serum stimulation, PKCζ (protein kinase C ζ) was found to phosphorylate SP1 and enhance its interaction with TEAD4. As a result, SP1 enhanced the transcriptional activity of YAP/TEAD and coregulated the expression of a group of YAP/TEAD target genes. The immune checkpoint V-domain Ig suppressor of T-cell activation (VISTA) was identified as a direct target of the SP1-YAP/TEAD4 complex and found to be widely expressed in CRC cells. Importantly, YAP-induced VISTA upregulation in human CRC cells was found to strongly suppress the antitumor function of CD8+ T cells. Consistently, elevated VISTA expression was found to be correlated with hyperactivation of the SP1-YAP/TEAD axis and associated with poor prognosis of CRC patients. In addition, we found by serendipity that enzymatic deglycosylation significantly improved the anti-VISTA antibody signal intensity, resulting in more accurate detection of VISTA in clinical tumor samples. Overall, our study identified SP1 as a positive modulator of YAP/TEAD for the transcriptional regulation of VISTA and developed a protein deglycosylation strategy to better detect VISTA expression in clinical samples. These findings revealed a new tumor cell-intrinsic mechanism of YAP/TAZ-mediated cancer immune evasion.

Humans↗