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Trutschl M.,One University Place | Kilgore P.C.S.R.,One University Place | Cvek U.,One University Place
Lecture Notes in Computer Science (including subseries Lecture Notes in Artificial Intelligence and Lecture Notes in Bioinformatics) | Year: 2013

Parallel coordinates has shown itself to be a powerful method of exploring and visualizing multidimensional data. However, applying this method to large datasets often introduces clutter, resulting in reduced insight of the data under investigation. We present a new technique that combines the classical parallel coordinates plot with a synthesized dimension that uses topological proximity as an indicator of similarity. We resolve the issue of over-plotting and increase the utility of the widely-used parallel coordinates visualization. © 2013 Springer-Verlag Berlin Heidelberg.

Mahdavian E.,One University Place | Palyok P.,One University Place | Adelmund S.,One University Place | Furmanski B.D.,Glaxosmithkline | And 5 more authors.
BMC Research Notes | Year: 2014

Results: Herein, we report that FC101 exhibits very potent in-vitro growth inhibitory effects (IC50ranging from 10nM-2.5 μM) against HaCat (pre-malignant skin), P9-WT (malignant skin), MCF-7 (low malignant breast), MDA-231 (malignant breast), SV-HUC (premalignant bladder), UM-UC14 (malignant bladder), and PC3 (malignant prostate) in a time-course and dose-dependent manner, with the UM-UC14 cells being the most sensitive. FC101 induces apoptosis and an increase in proportion of cells in the sub-G1 phase in both HaCat and P9-WT cell lines as evidenced by cell cycle profile analysis. In a mouse xenograft SCC tumor model, FC101 was well tolerated, non-toxic, and achieved a 30% reduction in tumor size at a dose of 8 mg/kg/day. FC101 is also a potent anti-angiogenenic agent. At nanomolar doses, FC101 inhibits the vascular endothelial growth factor-A (VEGF-A)-mediated proliferation of endothelial cells.Conclusions: Our data presented here indicates that FC101 is an excellent lead candidate for a small molecule anti-cancer agent that simultaneously affects angiogenesis signaling, cancer signal transduction, and apoptosis. Further understanding of the underlying FC101's molecular mechanism may lead to the design of novel targeted and selective therapeutics, both of which are pursued targets in cancer drug discovery.Background: Fusarochromanone (FC101) is a small molecule fungal metabolite with a host of interesting biological functions, including very potent anti-angiogenic and direct anti-cancer activity. © 2014 Mahdavian et al.; licensee BioMed Central Ltd.

Gade W.,One University Place | Schmit J.,One University Place | Collins M.,One University Place | Gade J.,One University Place
Clinical laboratory science : journal of the American Society for Medical Technology | Year: 2010

Metabolic syndrome (MSX) identifies clinical symptoms and lab results, including abdominal obesity, insulin resistance, hyperglycemia, hyperlipidemia, and hypertension, that lead to an increased risk of cardiovascular disease (CVD). Obesity typically results in insulin and leptin resistance and a shift from expansion of subcutaneous fat to deposition of abdominal and ectopic fat. These conditions cause metabolic dysregulation, elevated fatty acids (FFA), and increased secretion of pro-inflammatory "adipokines". Left untreated, these conditions cause lipotoxicity, chronic inflammation, hypertension, atherosclerosis, and CVD.

Gade W.,One University Place | Gade J.,One University Place | Collins M.,One University Place | Schmit J.,One University Place | Schupp N.,One University Place
Clinical laboratory science : journal of the American Society for Medical Technology | Year: 2010

From hot dogs to Hashimoto's and inheritance to inactivity, many "entrance ramps" converge onto the "Highway to Obesity", each contributing caloric intake that exceeds expenditure. Initially, the hypothalamus regulates appetite and energy based on leptin feedback, until feedback failure increases appetite, and allows deposition of abdominal fat, metabolic dysregulation, and metabolic syndrome. Without feedback controls, progress toward obesity is unimpeded unless diet, exercise, and/or medications provide an exit ramp.

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