ZNFX1 functions as a master regulator of epigenetically induced pathogen mimicry and inflammasome signaling in cancer.

DNA methyltransferase and poly (ADP-ribose) polymerase inhibitors (DNMTis, PARPis) induce a stimulator of interferon genes (STING)-dependent pathogen mimicry response (PMR) in ovarian and other cancers. Here, we showed that combining DNMTis and PARPis upregulates expression of the nucleic-acid sensor NFX1-type zinc finger-containing 1 protein (ZNFX1). ZNFX1 mediated induction of PMR in mitochondria, serving as a gateway for STING-dependent interferon/inflammasome signaling.

Serratia Infections in Burn Care.

Serratia marcescens is an opportunistic nosocomial pathogen with significant implications for burn care due to its multidrug resistance, virulence, and ability to colonize hospital environments. This retrospective study, conducted at an American Burn Association Verified Burn Centre, reviewed 22 cases of S. marcescens infections from 2015 to 2020.

Applying Natural Language Processing Techniques to Map Trends in Insomnia Treatment Terms on the r/Insomnia Subreddit: Infodemiology Study.

Background: People share health-related experiences and treatments, such as for insomnia, in digital communities. Natural language processing tools can be leveraged to understand the terms used in digital spaces to discuss insomnia and insomnia treatments.

Objective: The aim of this study is to summarize and chart trends of insomnia treatment terms on a digital insomnia message board.

Cerebral iron accumulation in multiple sclerosis: Pathophysiology and therapeutic implications.

Multiple sclerosis (MS) is a chronic autoimmune disorder of the central nervous system characterized by demyelination, neuroinflammation, and neurodegeneration. Recent studies highlight the role of cerebral iron (Fe) accumulation in exacerbating MS pathophysiology. Fe, essential for neural function, contributes to oxidative stress and inflammation when dysregulated, particularly in the brain's gray matter and demyelinated lesions.

Mitochondrial DNA lineages determine tumor progression through T cell reactive oxygen signaling.

Mitochondrial DNA (mtDNA) is highly polymorphic, and host mtDNA variation has been associated with altered cancer severity. To determine the basis of this mtDNA-cancer association, we analyzed conplastic mice with the C57BL/6J (B6) nucleus but two naturally occurring mtDNA lineages, and , where mitochondria generate more oxidative phosphorylation (OXPHOS)-derived reactive oxygen species (mROS). In a cardiac transplant model, Foxp3+ T regulatory (Treg) cells supported long-term allograft survival, whereas Treg cells failed to suppress host T effector (Teff) cells, leading to acute rejection.