The surge in plastic production has spurred a global crisis as plastic pollution intensifies, with microplastics and nanoplastics emerging as notable environmental threats. Due to their miniature size, these particles are ubiquitous across ecosystems and pose severe hazards as they are ingested and bioaccumulate within organisms. Although global plastic production has reached an alarming 400.
View Article and Find Full Text PDFObjective: To identify risk factors for clinically-important drowning-associated lung injury (ciDALI) in children.
Study Design: This was a cross-sectional study of children (0 through18 years) who presented to 32 pediatric emergency departments (EDs) from 2010 through 2017. We reviewed demographics, comorbidities, prehospital data, chest radiographs reports, and ED course from emergency medical services, medical, and fatality records.
The MYC proto-oncogene is upregulated in >60% of triple-negative breast cancers (TNBCs), it can directly promote tumor cell proliferation, and its overexpression negatively regulates anti-tumor immune responses. For all these reasons, MYC has long been considered as a compelling therapeutic target. However, pharmacological inhibition of MYC function has proven difficult due to a lack of a drug-binding pocket.
View Article and Find Full Text PDFExcessive macrophage activation and production of pro-inflammatory cytokines are hallmarks of the Cytokine Storm Syndrome (CSS), a lethal condition triggered by sepsis, autoimmune disorders, and cancer immunotherapies. While depletion of macrophages at disease onset protects from lethality in an infection-induced CSS murine model, patients are rarely diagnosed early, hence the need to characterize macrophage populations during CSS progression and assess the therapeutic implications of macrophage targeting after disease onset. In this study, we identified MHCIIF4/80Tim4 macrophages as the primary contributors to the pro-inflammatory environment in CSS, while CD206F4/80Tim4 macrophages, with an anti-inflammatory profile, become outnumbered.
View Article and Find Full Text PDFAge-related inflammation or inflammaging is a key mechanism that increases disease burden and may control lifespan. How adipose tissue macrophages (ATMs) control inflammaging is not well understood in part because the molecular identities of niche-specific ATMs are incompletely known. Using intravascular labeling to exclude circulating myeloid cells and subsequent single-cell sequencing with orthogonal validation, we define the diversity and alterations in niche resident ATMs through lifespan.
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