Technoeconomic analysis of five microalgae-to-biofuels processes of varying complexity

The economics surrounding five algae-to-fuels process scenarios were examined. The different processes modeled were as follows: an open pond producing either triacylglycerides (TAG) or free fatty acid methyl ester (FAME), a solar-lit photobioreactor producing either FAME or free fatty acids (FFA), and a light emitting diode irradiated (LED-lighted) photobioreactor producing TAG. These processes were chosen to represent both classical and esoteric approaches presented in the open literature. Viable (or suggested) processing techniques to liberate and purify (and convert) the microalgal triacylglycerides were then modeled to accompany each growth option. The investment and cost per kg of fuel or fuel precursor for each process was determined. The open pond produced TAG at ～$7.50/kg, while the process using the LED-lit photobioreactor produced TAG at ～$33/kg. The scenario containing the solar-lit photobioreactor produced FAME at ～$25/kg, while the open pond produced FAME at ～$4/kg. The scenario containing the solar-lit photobioreactor produced FFA at ～$29/kg. The open pond scenarios appear to be closest to the $1/kg pricepoint at this time, and thus are the most viable economic options. Future technological advancements that reduce the cost of bioreactor vessels, LED lighting, and solvent recovery, may reduce the oil production costs of these scenarios to a more attractive level.     

Imaging long-term fate of intramyocardially implanted mesenchymal stem cells in a porcine myocardial infarction model

The long-term fate of stem cells after intramyocardial delivery is unknown. We used noninvasive, repetitive PET/CT imaging with [(18)F]FEAU to monitor the long-term (up to 5 months) spatial-temporal dynamics of MSCs retrovirally transduced with the sr39HSV1-tk gene (sr39HSV1-tk-MSC) and implanted intramyocardially in pigs with induced acute myocardial infarction. Repetitive [(18)F]FEAU PET/CT revealed a biphasic pattern of sr39HSV1-tk-MSC dynamics; cell proliferation peaked at 33-35 days after injection, in periinfarct regions and the major cardiac lymphatic vessels and lymph nodes. The sr39HSV1-tk-MSC-associated [(18)F]FEAU signals gradually decreased thereafter. Cardiac lymphography studies using PG-Gd-NIRF813 contrast for MRI and near-infrared fluorescence imaging showed rapid clearance of the contrast from the site of intramyocardial injection through the subepicardial lymphatic network into the lymphatic vessels and periaortic lymph nodes. Immunohistochemical analysis of cardiac tissue obtained at 35 and 150 days demonstrated several types of sr39HSV1-tk expressing cells, including fibro-myoblasts, lymphovascular cells, and microvascular and arterial endothelium. In summary, this study demonstrated the feasibility and sensitivity of [(18)F]FEAU PET/CT imaging for long-term, in-vivo monitoring (up to 5 months) of the fate of intramyocardially injected sr39HSV1-tk-MSC cells. Intramyocardially transplanted MSCs appear to integrate into the lymphatic endothelium and may help improve myocardial lymphatic system function after MI.     

Topochemical distribution of lignin and hydroxycinnamic acids in sugar-cane cell walls and its correlation with the enzymatic hydrolysis of polysaccharides

Background  

Lignin and hemicelluloses are the major components limiting enzyme infiltration into cell walls. Determination of the topochemical distribution of lignin and aromatics in sugar cane might provide important data on the recalcitrance of specific cells. We used cellular ultraviolet (UV) microspectrophotometry (UMSP) to topochemically detect lignin and hydroxycinnamic acids in individual fiber, vessel and parenchyma cell walls of untreated and chlorite-treated sugar cane. Internodes, presenting typical vascular bundles and sucrose-storing parenchyma cells, were divided into rind and pith fractions.     

Genetic variation in wholesale carcass cuts predicted from digital images in cattle

The objective of this study was to quantify the genetic variation in carcass cuts predicted using digital image analysis in commercial cross-bred cattle. The data set comprised 38,404 steers and 14,318 heifers from commercial Irish herds. The traits investigated included the weights of lower value cuts (LVC), medium value cuts (MVC), high value cuts (HVC), very high value cuts (VHVC) and total meat weight. In addition, the weights of total fat and total bones were available on the steers. Heritability of carcass cut weights, within gender, was estimated using an animal linear model, whereas genetic and phenotypic correlations among cuts were estimated using a sire linear model. Carcass weight was included as a covariate in all models. In the steers, heritability ranged from 0.13 (s.e. = 0.02) for VHVC to 0.49 (s.e. = 0.03) for total bone weight, and in the heifers heritability ranged from 0.15 (s.e. = 0.04) for MVC to 0.72 (s.e. = 0.06) for total meat weight. The coefficient of genetic variation for the different cuts varied from 1.4% to 3.6%. Genetic correlations between the different cut weights were all positive and ranged from 0.45 (s.e. = 0.08) to 0.89 (s.e. = 0.03) in the steers, and from 0.47 (s.e. = 0.14) to 0.82 (s.e. = 0.06) in the heifers. Genetic correlations between the wholesale cut weights and carcass conformation ranged from 0.32 (s.e. = 0.06) to 0.45 (s.e. = 0.07) in the steers, and from 0.10 (s.e. = 0.12) to 0.38 (s.e. = 0.09) in the heifers. Genetic correlations between the same wholesale cut traits in steers and heifers ranged from 0.54 (s.e. = 0.14) for MVC to 0.79 (s.e. = 0.06) for total meat weight; genetic correlations between carcass weight and carcass classification for conformation and fat score in both genders varied from 0.80 to 0.87. The existence of genetic variation in carcass cut traits, coupled with the routine availability of predicted cut weights from digital image analysis, clearly shows the potential to genetically improve carcass value.     

Insulin modulates hippocampal activity-dependent synaptic plasticity in a N-methyl-d-aspartate receptor and phosphatidyl-inositol-3-kinase-dependent manner

Insulin and its receptor are both present in the central nervous system and are implicated in neuronal survival and hippocampal synaptic plasticity. Here we show that insulin activates phosphatidylinositol 3-kinase (PI3K) and protein kinase B (PKB), and results in an induction of long-term depression (LTD) in hippocampal CA1 neurones. Evaluation of the frequency-response curve of synaptic plasticity revealed that insulin induced LTD at 0.033 Hz and LTP at 10 Hz, whereas in the absence of insulin, 1 Hz induced LTD and 100 Hz induced LTP. LTD induction in the presence of insulin required low frequency synaptic stimulation (0.033 Hz) and blockade of GABAergic transmission. The LTD or LTP induced in the presence of insulin was N-methyl-d-aspartate (NMDA) receptor specific as it could be inhibited by alpha-amino-5-phosphonopentanoic acid (APV), a specific NMDA receptor antagonist. LTD induction was also facilitated by lowering the extracellular Mg(2+) concentration, indicating an involvement of NMDA receptors. Inhibition of PI3K signalling or discontinuing synaptic stimulation also prevented this LTD. These results show that insulin modulates activity-dependent synaptic plasticity, which requires activation of NMDA receptors and the PI3K pathway. The results obtained provide a mechanistic link between insulin and synaptic plasticity, and explain how insulin functions as a neuromodulator.     

N-acetylcysteine amide, a novel cell-permeating thiol, restores cellular glutathione and protects human red blood cells from oxidative stress

Oxidative stress plays an important role in the progression of neurodegenerative and age-related diseases, causing damage to proteins, DNA, and lipids. A novel thiol N-acetylcysteine amide (AD4), the amide form of N-acetylcysteine (NAC) and a Cu(2+) chelator, was assessed for its antioxidant and protective effects using human red blood cells (RBCs) as a model. AD4 was shown by flow cytometry to inhibit tert.-butylhydroxyperoxide (BuOOH)-induced intracellular oxidation in RBCs stained with the oxidant-sensitive probe 2',7'-dichlorofluorescein diacetate. In addition, AD4 retarded BuOOH-induced thiol depletion and hemoglobin oxidation. Restoration of the thiol-depleted RBCs by externally applied AD4 was significantly greater compared with NAC and, unlike NAC, was accompanied by hemoglobin protection from oxidation. In a cell-free system we have demonstrated that AD4 reacted with oxidized glutathione (GSSG) to generate reduced glutathione (GSH). The formation of GSH was determined enzymatically using GSH peroxidase and by HPLC. Based on these results a thiol-disulfide exchange between AD4 and GSSG is proposed as the mechanism underlying the antioxidant effects of AD4 on BuOOH-treated RBCs. Together, these studies demonstrate that AD4 readily crosses cell membranes, replenishes intracellular GSH, and, by incorporating into the redox machinery, defends the cell from oxidation. These results provide further evidence for the efficient membrane permeation of AD4 over NAC, and support the possibility that it could be explored for treatment of neurodegeneration and other oxidation-mediated disorders.     

Metazoan Scc4 homologs link sister chromatid cohesion to cell and axon migration guidance

Saccharomyces cerevisiae Scc2 binds Scc4 to form an essential complex that loads cohesin onto chromosomes. The prevalence of Scc2 orthologs in eukaryotes emphasizes a conserved role in regulating sister chromatid cohesion, but homologs of Scc4 have not hitherto been identified outside certain fungi. Some metazoan orthologs of Scc2 were initially identified as developmental gene regulators, such as Drosophila Nipped-B, a regulator of cut and Ultrabithorax, and delangin, a protein mutant in Cornelia de Lange syndrome. We show that delangin and Nipped-B bind previously unstudied human and fly orthologs of Caenorhabditis elegans MAU-2, a non-axis-specific guidance factor for migrating cells and axons. PSI-BLAST shows that Scc4 is evolutionarily related to metazoan MAU-2 sequences, with the greatest homology evident in a short N-terminal domain, and protein–protein interaction studies map the site of interaction between delangin and human MAU-2 to the N-terminal regions of both proteins. Short interfering RNA knockdown of human MAU-2 in HeLa cells resulted in precocious sister chromatid separation and in impaired loading of cohesin onto chromatin, indicating that it is functionally related to Scc4, and RNAi analyses show that MAU-2 regulates chromosome segregation in C. elegans embryos. Using antisense morpholino oligonucleotides to knock down Xenopus tropicalis delangin or MAU-2 in early embryos produced similar patterns of retarded growth and developmental defects. Our data show that sister chromatid cohesion in metazoans involves the formation of a complex similar to the Scc2-Scc4 interaction in the budding yeast. The very high degree of sequence conservation between Scc4 homologs in complex metazoans is consistent with increased selection pressure to conserve additional essential functions, such as regulation of cell and axon migration during development.