COMPOUNDS FOR INCREASING LIPID SYNTHESIS AND STORAGE

This invention relates to methods for increasing lipid production in cells. Methods of producing biofuel from cells and preparing mutraceuticals comprising lipids produced according to a method provided herein are also provided

Phenotypic screening identifies Brefeldin A/Ascotoxin as an inducer of lipid storage in the algae \u3ci\u3eChlamydomonas reinhardtii\u3c/i\u3e

The use of microalgae as a biofuel feedstock is highly desired, but current methods to induce lipid accumulation cause severe stress responses that limit biomass and, thus oil yield. To address these issues, a high throughput screening (HTS) method was devised to identify chemical inducers of growth and lipid accumulation. Optimization was performed to determine the most effective cell density, DMSO and Nile Red (NR) concentrations to monitor growth and lipid accumulation. The method was tested using 1717 compounds from National Cancer Institute (NCI) Diversity Set III and Natural Products Set II in Chlamydomonas reinhardtii. Cells were inoculated at low density and 10 μM of the test compound was added. After 72 h, cell density was measured at OD550 and lipid accumulation assessed using NR fluorescence. Primary screening identified 8 compounds with a hit rate of 0.47% and a robust Z′ discrimination factor (0.68 ± 0.1). Of these, Brefeldin A (BFA) was the most successful at inducing lipid accumulation and was used to evaluate secondary screens including measuring levels of fatty acids, photosynthetic pigments, proteins and carbohydrates. The effectiveness of BFA was confirmed in Chlorella sorokiniana UTEX 1230. This study demonstrates the power of chemical genomics approaches in biofuel research

Transcriptome analysis-identified long noncoding RNA CRNDE in maintaining endothelial cell proliferation, migration, and tube formation

Obesity is a leading risk factor for type-2 diabetes. Diabetes often leads to the dysregulation of angiogenesis, although the mechanism is not fully understood. Previously, long noncoding RNAs (lncRNAs) have been found to modulate angiogenesis. In this study, we asked how the expression levels of lncRNAs change in endothelial cells in response to excessive palmitic acid treatment, an obesitylike condition. Bioinformatics analysis revealed that 305 protein-coding transcripts were upregulated and 70 were downregulated, while 64 lncRNAs were upregulated and 46 were downregulated. Gene ontology and pathway analysis identified endoplasmic reticulum stress, HIF-1 signaling, and Toll-like receptor signaling as enriched after palmitic acid treatment. Moreover, we newly report enrichment of AGE-RAGE signaling pathway in diabetic complications, IL-17 signaling, and cysteine and methionine metabolism by palmitic acid. One lncRNA, Colorectal Neoplasia Differentially Expressed (CRNDE), was selected for further investigation. Palmitic acid induces CRNDE expression by 1.9-fold. We observed that CRNDE knockdown decreases endothelial cell proliferation, migration, and capillary tube formation. These decreases are synergistic under palmitic acid stress. These data demonstrated that lncRNA CRNDE is a regulator of endothelial cell proliferation, migration, and tube formation in response to palmitic acid, and a potential target for therapies treating the complications of obesityinduced diabetes

COMPOUNDS FOR INCREASING LIPID SYNTHESIS AND STORAGE

This invention relates to methods for increasing lipid production in cells. Methods of producing biofuel from cells and preparing mutraceuticals comprising lipids produced according to a method provided herein are also provided

Transcriptome analysis-identified long noncoding RNA CRNDE in maintaining endothelial cell proliferation, migration, and tube formation

Obesity is a leading risk factor for type-2 diabetes. Diabetes often leads to the dysregulation of angiogenesis, although the mechanism is not fully understood. Previously, long noncoding RNAs (lncRNAs) have been found to modulate angiogenesis. In this study, we asked how the expression levels of lncRNAs change in endothelial cells in response to excessive palmitic acid treatment, an obesitylike condition. Bioinformatics analysis revealed that 305 protein-coding transcripts were upregulated and 70 were downregulated, while 64 lncRNAs were upregulated and 46 were downregulated. Gene ontology and pathway analysis identified endoplasmic reticulum stress, HIF-1 signaling, and Toll-like receptor signaling as enriched after palmitic acid treatment. Moreover, we newly report enrichment of AGE-RAGE signaling pathway in diabetic complications, IL-17 signaling, and cysteine and methionine metabolism by palmitic acid. One lncRNA, Colorectal Neoplasia Differentially Expressed (CRNDE), was selected for further investigation. Palmitic acid induces CRNDE expression by 1.9-fold. We observed that CRNDE knockdown decreases endothelial cell proliferation, migration, and capillary tube formation. These decreases are synergistic under palmitic acid stress. These data demonstrated that lncRNA CRNDE is a regulator of endothelial cell proliferation, migration, and tube formation in response to palmitic acid, and a potential target for therapies treating the complications of obesityinduced diabetes

An evaluation of waste radiotoxicity reduction for a fast burner reactor closed fuel cycle: NEA benchmark results

As part of a program proposed by the OECD/NEA Working Party on Physics of Plutonium Recycling (WPPR) to evaluate different scenarios for the use of plutonium, fast reactor physics benchmarks were developed. In this paper, the fuel cycle performance of the metal-fueled benchmark is evaluated in detail. Benchmark results assess the reactor performance and toxicity behavior in a closed nuclear fuel cycle for a parametric variation of the conversion ratio between 0.5 and 1.0. Results indicate that a fast burner reactor closed fuel cycle can be utilized to significantly reduce the radiotoxicity destined for ultimate disposal