Project description:RATIONALE: Chemoprevention is the use of certain drugs to keep cancer from forming, growing, or coming back. The use of nitric oxide-releasing acetylsalicyclic acid may prevent colorectal cancer.
PURPOSE: This randomized phase I trial is studying the side effects and best dose of nitric oxide-releasing acetylsalicyclic acid in preventing colorectal cancer in patients at high risk of colorectal cancer.
Project description:Nitric oxide (NO) is implicated in the pathogenesis of various neuropathologies characterised by oxidative stress. NO has been reported to be involved in the exacerbation of oxidative stress by various mechanisms, including protein modification, genotoxic damage and elevated production of reactive oxygen species resulting in deregulation and disruption of cellular homeostasis. Although multiple roles for NO has been reported in neuronal death signaling, existent data fail to provide a holistic description of how nitrergic pathobiology elicits neuronal injury. Here we provide a comprehensive description of mechanisms contributing to NO-induced neuronal injury by global transcriptomic profiling.
Project description:In the present study, a distinct transcriptome regulated by NO2-CLA was revealed in primary human coronary artery endothelial cells (HCAECs) through RNA sequencing. Differential gene expression and pathway enrichment analysis identified numerous regulatory networks of cell cycle regulation, inflammation and redox responses, nitric oxide biosynthesis, hypoxia and chaperones in response to NO2-CLA, suggesting potent and diverse effects of NO2-CLA on cellular processes.
Project description:Nitric oxide (NO) is implicated in the pathogenesis of various neuropathologies characterised by oxidative stress. NO has been reported to be involved in the exacerbation of oxidative stress by various mechanisms, including protein modification, genotoxic damage and elevated production of reactive oxygen species resulting in deregulation and disruption of cellular homeostasis. Although multiple roles for NO has been reported in neuronal death signaling, existent data fail to provide a holistic description of how nitrergic pathobiology elicits neuronal injury. Here we provide a comprehensive description of mechanisms contributing to NO-induced neuronal injury by global transcriptomic profiling. Microarray analysis was carried out using 14 GeneChip Mouse Genome 430 2.0 array (Affymetrix, Santa Clara, CA). The assignment of the arrays (GeneChip) was as follows: vehicle-treated control (n=5); NOC-18-treatment for 8, 15 and 24 hour (n=3 for each time-point).
Project description:The dysfunction of endothelial nitric oxide synthase may be involved in development of atherosclerosis; however, the underlying molecular and cellular mechanisms of atherosclerosis are poorly understood. Here, we investigated gene expressionsin relation to atherosclerosis using endothelial nitric oxide synthase (eNOS)-deficient mice.
Project description:Our study represents the first detailed analysis of transcriptomes between poststroke anxiety and General Anxiety by RNA-seq technology. We founded that: compared with pure restraint stress, stroke plus restraint stress leaded to other pathways: 1) Oxidative stress and redox pathways are out-of-balance; 2). Production of nitric oxide is disordered; 3). Mitochondrial ATP synthesis is coupled with electron transport pathway dysfunction. These upregulated genes analyzed integrally were greatly enriched in the regulation of cytokine production, inflammatory response and leukocyte infiltration. And our results detailly predicted downstream transcriptional differences with HDAC3 inhibitor treatment or not in poststroke anxiety. We concluded that HDAC3-regulated PGE2 production by microglia constitutes phobic anxiety susceptibility after stroke.
Project description:Nitric oxide being a versatile molecule inside biological systems, from being both a cell signaling molecule to a potent stress agent, has significant effect in the transcriptional response in fission yeast. We have used fission yeast microarrays to identify cellular targets of Nitric Oxide (NO) and to further understand the cellular mechanism of NO action. We report the change in the global gene expression profile response to NO in S. pombe cells
