This study presents a facile one-pot solvothermal synthesis of high-performance green fluorescent carbon dots (G-CDs) using o-phenylenediamine and ethylenediamine as precursors. The G-CDs show excellent optical, temporal, and chemical stability. Notably, they exhibit the highest quantum yield of 24.
View Article and Find Full Text PDFAims: The NADPH oxidase (NOX) family of enzymes catalyzes the formation of reactive oxygen species (ROS). NOX enzymes not only have a key role in a variety of physiological processes but also contribute to oxidative stress in certain disease states. To date, while numerous small molecule inhibitors have been reported (in particular for NOX2), none have demonstrated inhibitory activity in vivo.
View Article and Find Full Text PDFHypoxia-inducible factor-1 (HIF-1), consisting of oxygen-sensitive HIF-1alpha and constitutively expressed HIF-1beta subunits, is a master transcriptional activator for cellular response to hypoxia. To explore direct HIF-1 targets, here we used differential gel electrophoresis (DIGE) to compare the HIF-1-regulated proteins between leukemic U937T-cell line with and without conditional induction of HIF-1alpha protein by tetracycline-off system. Among the upregulated proteins identified, mRNA levels of annexin A1, macrophage-capping protein (CapG), S100 calcium-binding protein A4 (S100A4), S100A11, acyl-CoA-binding protein and calcyclin-binding protein also increased.
View Article and Find Full Text PDFAm J Physiol Lung Cell Mol Physiol
October 2009
Angiotensin-converting enzyme (ACE) enhances the proliferation and migration of pulmonary artery smooth muscle cells (PASMCs), which contribute to the pathogenesis of hypoxic pulmonary hypertension (HPH). Previous reports have demonstrated that hypoxia upregulates ACE expression, but the underlying mechanism is unknown. Here, we found that ACE is persistently upregulated in PASMCs on the transcriptional level during hypoxia.
View Article and Find Full Text PDFWe previously reported that NSC606985, a new camptothecin analog, induces apoptosis of acute myeloid leukemic cells, which is triggered by proteolytic activation of protein kinase C delta (PKC delta). Here, we performed quantitative proteomic analysis of NSC606985-treated and untreated leukemic U937 cells with two-dimensional fluorescence difference gel electrophoresis (2-D DIGE) in combination with matrix-assisted laser desorption/ionization time-of-flight/time-of-flight tandem mass spectrometry. Thirty-three proteins were found to be deregulated.
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