Radial intralesional linear calcifications and focal hyperostosis: key points for diagnosis, extension and point of origin identification of sinonasal inverted papilloma.

Sinonasal inverted papilloma (IP) often appears as a unilateral sinonasal soft-tissue mass with varying enhancement, often accompanied by bone remodelling, intralesional calcifications, focal hyperostosis, and cone-shaped bone thickening (observed in 60 to 80% of cases) (1,2). A non-contrast sinonasal CT scan may reveal a soft tissue polypoid mass that closely resembles inflammatory polyps (Figure 1 A-D). While hyperostosis is recognized as a marker of the tumor's point of origin (1), intralesional calcifications are less frequently described but may offer valuable insights.

Upregulation of RNA Processing Factors in Poorly Differentiated Lung Cancer Cells.

Intratumoral heterogeneity in non-small cell lung cancer (NSCLC) has been appreciated at the histological and cellular levels, but the association of less differentiated pathology with poor clinical outcome is not understood at the molecular level. Gene expression profiling of intact human tumors fails to reveal the molecular nature of functionally distinct epithelial cell subpopulations, in particular the tumor cells that fuel tumor growth, metastasis, and disease relapse. We generated primary serum-free cultures of NSCLC and then exposed them to conditions known to promote differentiation: the air-liquid interface (ALI) and serum.

Identification of aldehyde dehydrogenase 1A1 modulators using virtual screening.

The highly similar aldehyde dehydrogenase isozymes (ALDH1A1 and ALDH2) have been implicated in the metabolism of toxic biogenic aldehydes such as 3,4-dihydroxyphenylacetaldehyde (DOPAL) and 4-hydroxy-2E-nonenal. We report the down-regulation of ALDH1A1 mRNA found in substantia nigra tissue of human Parkinson's disease (PD) samples using the Genome-Wide SpliceArray(™) (GWSA(™)) technology. Since DOPAL can rapidly inactivate ALDH1A1 in vitro, we set up a DOPAL-induced ALDH1A1 inactivation assay and used this assay to demonstrate that Alda-1, a compound originally identified as an activator of ALDH2, can also activate ALDH1A1.

Differential effects of PPARgamma ligands on oxidative stress-induced death of retinal pigmented epithelial cells.

Purpose: To investigate the role of the peroxisome proliferator-activated receptor (PPAR)-γ in modulating retinal pigmented epithelium (RPE) responses to oxidative stress.

Methods: ARPE-19 cells were treated with the oxidant, t-butylhydroperoxide (tBH) to induce apoptosis. Cells pretreated with synthetic PPARγ agonists of the antidiabetic thiazolidinediones class before tBH challenge were assessed for viability and, by microarray analysis, for effects on gene expression.