A One Health view of antimicrobial resistance in North Africa: Meta-analysis of ESBL-producing Enterobacteriaceae across sectors.

Enrichment of high-risk antibiotic resistance genes on microplastics in freshwater environments: A meta-analysis.

Direct observation of thermal interface vicinity effect and determination of thermal interface resistance by modified Angstrom method

Advancing precision medicine in pancreatic cancer using novel biomarkers and clinical targets.

Tumor-associated cells primarily comprise immune cells and stromal cells, which collectively construct tumor microenvironment (TME) through complex interactions. This environment not only accelerates tumor immune escape but also leads to chemotherapy resistance and immunotherapy failure, significantly increasing the risk of tumor progression and metastasis. Fortunately, these cells often exhibit phenotypic heterogeneity, allowing reprogramming strategies to transform their anti-tumor phenotypes into pro-tumor ones, thereby exerting beneficial regulatory effects on tumor progression. Nanodelivery systems (NDSs) offer significant advantages such as precise targeting and efficient delivery, making them crucial for implementing reprogramming strategies. Consequently, utilizing NDSs to reprogram tumor-associated cells for enhanced tumor therapy presents a promising solution. This review innovatively summarizes the fundamental roles, functional phenotypes, and diverse reprogramming strategies for immune cells and stromal cells within the TME. It then details therapeutic approaches by targeting distinct tumor-associated immune cells and stromal cells. Furthermore, it discusses the opportunities and challenges NDSs-based on reprogramming strategies to achieve cellular phenotype conversion. This review aims to advance our understanding of reprogramming tumor-associated immune or stromal cell phenotypes to enhance tumor therapy. STATEMENT OF SIGNIFICANCE: The tumor microenvironment (TME), largely orchestrated by heterogeneous populations of immune and stromal cells, is a pivotal determinant of therapeutic resistance and disease progression. Reprogramming these tumor-associated cells from pro-tumorigenic to anti-tumorigenic phenotypes represents a transformative strategy to overcome immune evasion, chemotherapy resistance, and immunotherapy failure. This review underscores the critical innovation of leveraging nanodelivery systems (NDSs) to precisely and efficiently implement such reprogramming strategies. By systematically synthesizing the roles, phenotypic states, and reprogramming approaches for key cellular components within the TME, this work provides a comprehensive framework for advancing targeted nanomedicine. It not only elucidates current therapeutic paradigms but also critically examines the prospects and challenges of integrating NDSs to achieve phenotypic conversion, thereby offering essential insights for the development of next-generation, microenvironment-focused cancer therapies.

Determination of plasma resistance based on the analysis of the noise component amplitude of the Langmuir probe current dependence on voltage

The emerging threat of multidrug-resistant (MDR) Acinetobacter (A.) species, coupled with limited data on its prevalence, resistance mechanisms, and genomic profiles in Nigeria, necessitates immediate study. This investigation characterized the microbial traits and genetic variation of Acinetobacter species isolated from human, animal, and environmental sources, with emphasis on resistance dynamics, virulence, inter-source relatedness and diversity in Lagos, Nigeria. From April 2023 to March 2024, 2835 samples were collected (1410 human, 1020 animal, and 405 environmental), processed, and the isolates were identified by classical microbiological methods. Further identification was carried out by Matrix-Assisted Laser Desorption Ionization-Time of Flight (MALDI-TOF) mass spectrometry and confirmed by Whole Genome Sequencing (WGS). Antibiotic susceptibility testing (AST) was assessed by the microdilution method using the MICRONAUT system. WGS data were utilized for analyzing virulence factors, antimicrobial resistance (AMR) determinants, and phylogenetic lineages. Nineteen isolates were confirmed as Acinetobacter by MALDI-TOF and WGS, of which 14 were A. nosocomialis and five were A. junii. The AST results revealed that both Acinetobacter species exhibited 100% resistance to cefotaxime and fosfomycin, while 100% of A. nosocomialis were resistant to chloramphenicol. Genomic analysis revealed that all A. nosocomialis isolates harbored 21 intrinsic AMR genes, including four distinct bla ADC variants and 17 efflux-related genes, which were all absent in A. junii. Moreover, A. nosocomialis harbored 68 virulence genes spanning seven mechanisms, compared to six virulence genes spanning five mechanisms in A. junii, with the absence of exotoxin and biofilm formation mechanisms. Both species have six conserved virulence-associated genes [ompA, ACICU_RS00500, bfmR, pilG, pilT, and vgrG/tssI], and two distinct plasmids were exclusively detected in A. nosocomialis. Phylogenomic analysis demonstrated that both species formed distinct sub-clusters from different sources, suggesting shared evolutionary or transmission contexts. For example, five isolates (three A. nosocomialis from cattle nasal swab, human sputum, and abattoir effluent) and two A. junii from cattle rectal swab, and cattle nasal swab) form a distinct cluster differing by 15 SNP, indicating potential cross-species dynamics warranting deeper investigation. This study revealed the existence of A. nosocomialis and A. junii resistant to cefotaxime and fosfomycin in the One Health sector in Lagos. Both species were found to exhibit six conserved virulence genes linked to pathogenicity. Advanced molecular diagnostics is needed to monitor the emergence and spread of virulence and antibiotic-resistance in Acinetobacter species in Nigeria.

Plant resistance influences the host range of pathogens; however, the mechanism driving this influence remains poorly understood. Brassicaceae species are not natural hosts of potexviruses, for reasons that have not yet been determined. This study investigated the molecular basis of nonhost resistance (NHR) to potexviruses in the Brassicaceae, focusing on the non-nucleotide-binding leucine-rich repeat (NLR) resistance gene JACALIN-TYPE LECTIN REQUIRED FOR POTEXVIRUS RESISTANCE1 (JAX1). We found that JAX1 is a Brassicaceae-specific conserved gene that has been lost or pseudogenized in some species, and duplicated in others. Most JAX1 orthologs from diverse Brassicaceae species effectively inhibit plantago asiatica mosaic virus (PlAMV) accumulation, indicating that antiviral activity is conserved among the Brassicaceae. However, we demonstrated that some Brassicaceae plants in which JAX1 expression was not detected allow local or systemic viral infection. Quadruple knockout of JAX1 genes via gene editing in Sisymbrium irio, a nonhost of PlAMV, led to loss of resistance and potexvirus susceptibility in this species. These results clearly indicate that JAX1 represents one layer of multi-layer NHR against potexviruses in the Brassicaceae, shedding light on the pivotal role of non-NLR antiviral resistance in shaping the host range of these plant viruses.

Here, we present whole genome sequencing (WGS) data of clinical Klebsiella pneumoniae and K. quasipneumoniae isolates obtained from urine samples collected between October 2024 and January 2025 from patients in hospitals in Baghdad, Iraq. A total of 30 K. pneumoniae isolates were initially recovered and screened using antimicrobial susceptibility testing, from which one carbapenem-resistance isolate (isolate 5) and one carbapenem- susceptible isolate (isolate 6) were selected for genome sequencing. Genomic DNA was extracted, sequenced using the illumine MiSeq platform, and assembled de novo. The resulting genome assembled were annotated using NCBI prokaryotic genome annotation pipeline and further analysed using the PATRIC platform. The dataset includes annotated genome assemblies with identified carbapenemase genes (including blaNDM-5, blaOXA-48, and blaOXA-181), additional antimicrobial resistance determinants, predicted virulence-associated genes, mobile genetic elements, and multilocus sequence typing results. Isolate 5 was assigned to sequence type ST14 (K. pneumoniae), while isolate 6 was assigned to ST7604 (K. quasipneumoniae). These genome data provide a curated genomic resource that can be reused for comparative genomics, antimicrobial resistance surveillance, and phylogenomic analysis of Klebsiella species from clinical setting in Iraq.

Understanding the probiotic potential of a healthy human vaginal flora, Lactobacillus gasseri K9: genomic and in vitro aspects

Characterization of antimicrobial resistance and biofilm formation in Escherichia coli isolated from wild boars.

Virulence and antimicrobial resistance profiling of Klebsiella pneumoniae isolated from foxes in northern China.

This dataset presents the draft genome of Ochrobactrum anthropi strain Nas42, isolated from metal-contaminated estuarine sediments of the Red River Delta, Vietnam. Genomic DNA was extracted from the isolate and sequenced using the Illumina MiSeq platform, followed by de novo assembly and functional annotation. The generated dataset comprises a 4,605,092 bp draft genome assembled into 27 contigs with a GC content of 56.11%, containing 4,356 protein-coding sequences. Notably, in silico whole-genome comparison supported its taxonomic assignment to O. anthropi , demonstrating 99.37% Average Nucleotide Identity (ANI) with strain PBO and the absence of IS711 insertion sequences, a genomic feature characteristic of Brucella species but absent in Ochrobactrum . Additionally, the annotated dataset highlights 45 genes associated with metal resistance, including those encoding resistance to cobalt, zinc, cadmium, and copper. This genomic resource can be reused by the scientific community to investigate metal resistance determinants, explore microbial adaptation mechanisms in polluted estuarine environments, and support phylogenomic analyses of the Ochrobactrum–Brucella complex.

Tackling antibiotic resistance in ESKAPE pathogens through the lens of bacterial small RNAs.

Interconnected reservoirs and escalating resistance in multidrug-resistant Pseudomonas aeruginosa: An One Health review.

Genomic characterization and global lineage-plasmid context of a bla NDM-5-harboring Escherichia coli ST3014 isolate.

This study aimed to genomically characterize clinical Enterococcus faecalis and Staphylococcus epidermidis isolates obtained from aspirate and sputum samples at Bayburt State Hospital, focusing on antimicrobial resistance genes, virulence factors, and mobile genetic elements. Whole-genome sequencing (WGS) was performed on the isolates, and antimicrobial resistance genes, virulence determinants, multilocus sequence types (MLST), plasmid replicons, and mobile genetic elements were identified using bioinformatics tools. The E. faecalis E5 (ST64) isolate, recovered from an aspirate sample, carried multiple antimicrobial resistance genes, including mecA, vanT, erm(B), tet(M), and qacA, along with a diverse virulence gene repertoire (cyl, ebp, ace, and agg), mobile genetic elements (Tn6009, ISL1a3), and four plasmid replicons (rep19C, rep9C, repUS43, and rep7a). The E. faecalis E184 and E187 isolates (ST124), obtained from sputum samples, harbored fewer acquired resistance genes but shared gyrA (T672A) and parC (V307I) mutations associated with fluoroquinolone resistance. The S. epidermidis ST59 isolate carried resistance genes lnu(A), fosB, and qacD, together with the plasmid replicon rep7a and insertion sequence ISSau4. The co-occurrence of lnu(A) and the rep7a plasmid in both species suggests a potential pathway for interspecies transmission of resistance determinants. This study reports the genomic detection of mecA in an E. faecalis isolate from Türkiye based on WGS analysis. However, this finding is based solely on genomic data and lacks phenotypic or experimental validation. The detection of a shared plasmid-associated resistance element (lnu(A)-rep7a) in both E. faecalis and S. epidermidis highlights the potential for interspecies resistance gene flow within the hospital environment.

Although 40-70% of TNBC cases overexpress EGFR, clinical responses to EGFR-targeted therapies have been minimal. This poor efficacy may result from intrinsic resistance mechanisms, inactive EGFR signaling, or reduced EGFR localization on the plasma membrane. To identify genetic determinants of EGFR inhibitor resistance, we performed a genome-wide CRISPR/Cas9 knockout screen in MDA-MB-231 cells. The screen revealed that loss of the redox-regulating enzyme Thioredoxin Reductase 3 (TXNRD3) sensitized TNBC cells to the EGFR inhibitor erlotinib. Functional validation showed that both siRNA-induced knockdown and pharmacological inhibition of TXNRD3 with the FDA-approved drug auranofin significantly enhanced the cytotoxic effects of EGFR inhibitors in EGFR-high TNBC cells. Mechanistically, TXNRD3 depletion or inhibition increased intracellular reactive oxygen species (ROS), leading to oxidation-dependent activation and phosphorylation of EGFR (Y1068) and subsequent activation of downstream signaling pathways in TNBC cells that otherwise lack active EGFR. The combined treatment of auranofin and EGFR inhibitors triggered GSDME-mediated pyroptosis in a ROS-dependent manner. Importantly, the combination of auranofin with erlotinib exhibited potent anti-tumor efficacy in vivo in both MDA-MB-231 xenograft and 4T1.2 syngeneic TNBC models. Collectively, our findings identify TXNRD3 as a redox-dependent regulator of EGFR activity and drug response in TNBC and demonstrate that auranofin-mediated TXNRD3 inhibition can re-activate EGFR signaling, thereby sensitizing TNBC tumors to EGFR-targeted therapy. This study provides a mechanistic rationale for repurposing auranofin in combination with EGFR inhibitors as a novel therapeutic strategy for EGFR-high TNBCs.

Antimicrobial resistance in Neisseria gonorrhoeae is an urgent threat to public health. Recent reports have highlighted the continued rise in ceftriaxone resistance, our last-line empiric treatment option. Molecular assays that detect the genetic determinants of resistance can improve antibiotic stewardship and increase the therapeutic options for cases of gonorrhea. As a result, those tests can reduce the pressure toward the emergence of ceftriaxone resistance. However, most molecular assays cannot be deployed in low-resource settings due to a lack of infrastructure. We report on the development of a point-of-care assay for predicting resistance to an oral first-line treatment option, cefixime. The assay provided results in under 30 min and demonstrated strong correlation with phenotypic and genotypic resistance. Furthermore, we report on the proof-of-concept freeze-drying of assay reagents, which could permit cold-chain-independent use. Collectively, our study provides the groundwork for developing and deploying such molecular resistance assays in low-resource settings.

Klebsiella variicola is an emerging multidrug‑resistant opportunistic pathogen that is often misidentified as K. pneumoniae in clinical laboratories. Here, we investigated four NDM‑9-producing K. variicola ST363‑KL151 isolates from patients treated at a tertiary-care centre in China. Whole-genome sequencing and genomic analyses were performed to confirm species identity, define molecular characteristics, and identify resistance determinants. Core-genome SNP analysis was used to assess phylogenetic relatedness to international strains. Carbapenem-resistance transferability was evaluated by conjugation to E. coli. Biofilm formation, epithelial-cell invasion/cytotoxicity, serum bactericidal resistance, and virulence in a Galleria mellonella infection model were assessed. Antimicrobial susceptibility testing revealed a broad resistance profile encompassing β‑lactams (including carbapenems), aminoglycosides, fluoroquinolones, and fosfomycin, while retaining susceptibility to tigecycline. One isolate demonstrated elevated polymyxin resistance with an MIC of 64mg/L, mediated by mgrB truncation (p.Gln30*). Whole‑genome sequencing identified a IncHI2A plasmid carrying a unique IS26‑flanked blaNDM‑9 composite transposon adjacent to a mercury resistance operon, and conjugation assays confirmed transferable carbapenem resistance. Phylogenetic analysis placed the ST363-KL151 isolates in a monophyletic clade with a Norwegian strain collected in 2015. Although hypervirulence plasmids and classical virulence loci were absent, the isolates showed substantial biofilm formation and serum resistance, but only moderate cytotoxicity in epithelial cells and limited lethality in Galleria mellonella compared with the hypervirulent control NTUH-K2044. These findings identify NDM‑9‑producing K. variicola ST363‑KL151 as a multidrug‑resistant lineage, emphasizing the need for accurate species identification and genome‑based surveillance to prevent its further clinical spread.