Posterior reversible encephalopathy syndrome (PRES) is a rapidly progressive neurologic condition presenting with typical symptoms including headache, nausea, vomiting, altered mental status, and visual defects. Neuroimaging profile, particularly magnetic resonance imaging (MRI), is the most important tool for diagnosis. The most commonly reported etiological factors include hypertensive emergency and renal disease. We describe a 67-year-old lady who developed clinical and radiological characteristics of PRES secondary to Varicella encephalitis.
Interferon regulatory factor 1 (IRF1) regulates diverse biological functions, including modulation of cellular responses involved in tumorigenesis. Genetic mutations and altered IRF1 function are associated with several cancers. Although the function of IRF1 in the immunobiology of cancer is emerging, IRF1-specific mechanisms regulating tumorigenesis and tissue homeostasis in vivo are not clear. Here, we found that mice lacking IRF1 were hypersusceptible to colorectal tumorigenesis. IRF1 functions in both the myeloid and epithelial compartments to confer protection against AOM/DSS-induced colorectal tumorigenesis. We further found that IRF1 also prevents tumorigenesis in a spontaneous mouse model of colorectal cancer. The attenuated cell death in the colons of Irf1–/–mice was due to defective pyroptosis, apoptosis, and necroptosis (PANoptosis). IRF1 does not regulate inflammation and the inflammasome in the colon. Overall, our study identified IRF1 as an upstream regulator of PANoptosis to induce cell death during colitis-associated tumorigenesis.
The study of the interaction of engineered nanoparticles, including quantum dots (QDs), with cellular constituents and the kinetics of their localization and transport, has provided new insights into their biological consequences in cancers and for the development of effective cancer therapies. The present study aims to elucidate the toxicity and intracellular transport kinetics of CdSe/ZnS and InP/ZnS QDs in late-stage ML-1 thyroid cancer using well-tested HeLa as a control. Our XTT (2,3-bis-(2-methoxy-4-nitro-5-sulfophenyl)-2H-tetrazolium-5-carboxanilide) viability assay (Cell Proliferation Kit II) showed that ML-1 cells and non-cancerous mouse fibroblast cells exhibit no viability defect in response to these QDs, whereas HeLa cell viability decreases. These results suggest that HeLa cells are more sensitive to the QDs compared to ML-1 cells. To test the possibility that transporting rates of QDs are different between HeLa and ML-1 cells, we performed a QD subcellular localization assay by determining Pearson’s Coefficient values and found that HeLa cells showed faster QDs transporting towards the lysosome. Consistently, the ICP-OES test showed the uptake of CdSe/ZnS QDs in HeLa cells was significantly higher than in ML-1 cells. Together, we conclude that high levels of toxicity in HeLa are positively correlated with the traffic rate of QDs in the treated cells.