Wanmeng Xiao

Ionizing radiation is a common therapy for solid tumors, but it concurrently damages normal tissues,1 leading to adverse effects such as acute radiation syndrome (ARS).2 Hematopoietic injury is a p...

Accumulating evidence highlights the pivotal role of microbiomes in cancer development. To elucidate the esophageal microbiome’s characteristics during esophageal squamous cell carcinoma (ESCC) progression, normal tissues from 13 healthy controls (HC), paired esophageal squamous intraepithelial neoplasia (ESIN) lesional and adjacent (ESINA) tissues from 10 ESIN individuals, and ESCC lesional and adjacent (ESCCA) tissues from 12 ESCC individuals were collected. Following 16S rRNA and ITS sequencing, analyses encompassed α/β-diversity assessments, shared species identification, Type-I Taylor’s Power Law Extensions (TPLE), linear discriminant analysis effect size (LEfSe), co-occurrence networks, receiver operating characteristic (ROC) curve analysis, and functional predictions. Distinct microbial signatures characterized HC, precancerous, and cancerous groups. The ESIN group exhibited unique microbial features, including diminished bacterial and fungal species sharing relative to the ESINA group and maximal b values in TPLE for both taxa. Despite the absence of significant bacterial composition differences between HC and ESIN in β-diversity analysis, notable alterations in the oral microbiome were observed. ESIN was marked by Lactobacillus and Aspergillus enrichment, while ESCC was predominantly associated with Fusobacterium , Streptococcus , and Alternaria . Disease progression led to shifts and reductions in species co-occurrence network interactions. Aspergillus demonstrated potential diagnostic value for ESIN, and its ratio to pathogenic functional clusters within network analysis significantly enhanced ESCC detection accuracy. Functional predictions revealed stage-specific pathway enrichments. These findings delineate microbiome alterations across ESCC stages, emphasizing ESIN-specific microbial shifts that may inform microbiome-based strategies for early detection and intervention. IMPORTANCE: This study collected esophageal tissues through gastroscopic biopsy and conducted sequencing and analyses to explore the diversity, heterogeneity, key microbial composition, interaction networks, and functional predictions of resident bacteria and fungi in esophageal squamous cell carcinoma (ESCC) progression. The esophageal squamous intraepithelial neoplasia group showed the highest heterogeneity in oral microbiome and fungi, with certain species potentially contributing to ESCC progression. Targeting the oral microbiome in high-risk populations may thus provide a valuable approach for improving early diagnosis and potentially intervening in disease progression.

Sepsis is a life-threatening condition characterized by systemic organ dysfunction caused by a cytokine storm mediated by inflammatory mediators. Antibacterial gold nanoclusters (AuDAMP) were synthesized via a one-pot method. The therapeutic efficacy of AuDAMP was systematically evaluated in two sepsis mouse models: the cecum ligation and puncture (CLP) model and the lipopolysaccharide (LPS)-induced sepsis-associated acute lung injury model. Remarkably, AuDAMP demonstrated potent anti-septic effects through antimicrobial activity and attenuation of the cytokine storm. Furthermore, AuDAMP exhibited synergistic therapeutic effects when combined with meropenem, suggesting great potential as a novel therapeutic strategy for sepsis management.

Introduction: Despite observational studies suggest hypotheses indicating a potential link, the precise causal connection between sarcopenia and digestive system illnesses has not been clearly defined.Methods: We first use Linkage Disequilibrium Score Regression (LDSC) testing to determine the genetic correlation of traits associated with sarcopenia and 10 specific gastrointestinal diseases. Subsequently, we performed a set of bidirectional Mendelian Randomization (MR) analyses to gauge the genetic inclination towards sarcopenia-related traits in relation to each gastrointestinal condition, individually, across the FinnGen, UK Biobank, and other extensive collaborative consortia. The analytical outcomes were synthesized using a fixed-effects meta-analytic model. For outcomes indicating substantial causal impacts, mediation MR analyses were executed. Additionally, a battery of sensitivity analyses was conducted to evaluate the study’s strength and dependability.Results: Our findings established a strong causal link between appendicular lean mass and gastroesophageal reflux disease (OR = 0.8607; 95% CI: 0.8345–0.8877; p < 0.0001) and a noteworthy correlation with nonalcoholic fatty liver disease (OR = 0.7981; 95% CI: 0.7281–0.8749; p < 0.0001), as per the meta-analysis data. We also evaluated the intermediary role of metabolic disorders in the association between appendicular lean mass and the aforementioned diseases. The intermediary effect towards gastroesophageal reflux disease is quantified as 0.0087 (95% CI, 8e-04, 0.0183), accounting for 5.9398% (95% CI, 0.5462, 12.4940%) of the overall effect. For non-alcoholic fatty liver, the intermediary impact is 0.0150 (95% CI, 0.0050, 0.0270), representing 19.7808% (95% CI, 6.5936, 35.6055%) of the total effect.Conclusion: The findings posit that augmenting muscle mass may serve as a preventative strategy against gastroesophageal reflux disease and non-alcoholic fatty liver, highlighting the critical role of metabolic disorder management in reducing the risks of these sarcopenia-related conditions.