Energy From Biochemical Sources

As available energy reserves decline, renewable sources must be utilized. Organic matter, grown agriculturally, represents a renewable energy source, which is readily available. This paper reviews the methods by which organic matter can be converted to energy sources by biochemical processes. The economics of conversion of agricultural crops and byproducts to alcohols by fermentation and conversion of these agricultural materials to methane by anaerobic digestion are examined. Projections of the potential of this energy source are quite promising

Genotype by environment interactions for growth in Red Angus

Citation: Fennewald, D. J., Weaber, R. L., & Lamberson, W. R. (2017). Genotype by environment interactions for growth in Red Angus. Journal of Animal Science, 95(2), 538-544. doi:10.2527/jas2016.0846Accuracy of sire selection is limited by how well animals are characterized for their environment. The objective of this study was to evaluate the presence of genotype x environment interactions (GxE) for birth weight (BiW) and weaning weight (WW) for Red Angus in the United States. Adjusted weights were provided by the Red Angus Association of America. Environments were defined as 9 regions within the continental United States with similar temperature-humidity indices. Mean weights of calves were determined for each region and for each sire's progeny within each region. A reaction norm (RN) for each bull was estimated by regressing the sire means on the region means weighted for the number of progeny of each sire. The range for BiW and WW RN was -1.3 to 4.0 and -1.7 to 2.8, respectively. The heritabilities of BiW and WW RN were 0.40 and 0.39, respectively. Phenotypic and genetic correlations between BiW and WW RN were 0.19 and 0.54, respectively. The phenotypic correlation of the progeny mean to the RN was -0.20 (P < 0.05) and suggests that sires with higher means are more stable in progeny performance across environments. Weights in different regions were considered separate traits and genetic correlations were estimated between all pairs of regions as another method to determine GxE. Genetic correlations < 0.80 indicate GxE at a level for concern, but existed for only 2 of 36 estimates for BiW and 12 of 36 estimates for WW. Genetic correlations between different regions ranged from 0.74 to 0.96 for BiW and 0.62 to 0.99 for WW and indicate that sires tend to rank similarly across environments for these traits

Genetic Diversity of EBV-Encoded LMP1 in the Swiss HIV Cohort Study and Implication for NF-Κb Activation

Epstein-Barr virus (EBV) is associated with several types of cancers including Hodgkin's lymphoma (HL) and nasopharyngeal carcinoma (NPC). EBV-encoded latent membrane protein 1 (LMP1), a multifunctional oncoprotein, is a powerful activator of the transcription factor NF-κB, a property that is essential for EBV-transformed lymphoblastoid cell survival. Previous studies reported LMP1 sequence variations and induction of higher NF-κB activation levels compared to the prototype B95-8 LMP1 by some variants. Here we used biopsies of EBV-associated cancers and blood of individuals included in the Swiss HIV Cohort Study (SHCS) to analyze LMP1 genetic diversity and impact of sequence variations on LMP1-mediated NF-κB activation potential. We found that a number of variants mediate higher NF-κB activation levels when compared to B95-8 LMP1 and mapped three single polymorphisms responsible for this phenotype: F106Y, I124V and F144I. F106Y was present in all LMP1 isolated in this study and its effect was variant dependent, suggesting that it was modulated by other polymorphisms. The two polymorphisms I124V and F144I were present in distinct phylogenetic groups and were linked with other specific polymorphisms nearby, I152L and D150A/L151I, respectively. The two sets of polymorphisms, I124V/I152L and F144I/D150A/L151I, which were markers of increased NF-κB activation in vitro, were not associated with EBV-associated HL in the SHCS. Taken together these results highlighted the importance of single polymorphisms for the modulation of LMP1 signaling activity and demonstrated that several groups of LMP1 variants, through distinct mutational paths, mediated enhanced NF-κB activation levels compared to B95-8 LMP1

Alterations in NF-κB and RBP-Jκ by Arenavirus Infection of Macrophages In Vitro and In Vivo

Pichinde virus is an arenavirus that infects guinea pigs and serves as an animal model for human Lassa fever. An attenuated Pichinde virus variant (P2) and a virulent variant (P18) are being used to delineate pathogenic mechanisms that culminate in shock. In guinea pigs, the infection has been shown to begin in peritoneal macrophages following intraperitoneal inoculation and then spreads to the spleen and other reticuloendothelial organs. We show here that infection of the murine monocytic cell line P388D1 with either Pichinde virus variant resulted in the induction of inflammatory cytokines and effectors, including interleukin-6 and tumor necrosis factor alpha. Since these genes are regulated in part by the cellular transcription factors NF-κB and RBP-Jκ, we compared the activities of NF-κB and RBP-Jκ in P388D1 cells following infection with Pichinde virus. The attenuated P2 virus inhibited NF-κB activation and caused a shift in the size of the RBP-Jκ complex. The virulent P18 virus showed less inhibition of NF-κB and failed to alter the size of the RBP-Jκ complex. Peritoneal cells from P2-infected guinea pigs showed induction of NF-κB RelA/p50 heterodimer and p50/p50 homodimer and manifested an increase in the size of RBP-Jκ. By contrast, P18 induced large amounts of the NF-κB p50/p50 dimer but failed to induce RelA/p50 or to cause an increase in the RBP-Jκ size. Taken together, these changes suggest that the attenuated viral strain induces an “activation” of macrophages, while the virulent form of the virus does not