Decarboxylating free fatty acids into fuels using subcritical water

Biofuel producers are looking into new avenues for utilization of their byproducts to improve their profitability in an environmentally friendly way. The biodiesel market has become saturated with very low margins and blenders cannot utilize this product in the winter. In order to address this problem, attention has now shifted towards a range of other possible products that can be made from non-food grade byproduct oils, including green diesel (a diesel having the same analytical signature as petroleum diesel), jet fuels, and other high value products. The major goal of this work was to investigate the hydrothermal conversion of bio-oil to fuel grade hydrocarbons as green diesel. Oleic acid was selected as a model compound of bio-oil to understand the reaction chemistry. Hydrothermal reactions were carried out in a CSTR (batch mode) from 300 to 450oC and reaction time was varied from 10 minutes to 6 hours. GC-FID and GC-TCD were used to analyze the liquid and gas samples, respectively. GC-TCD results showed that decarboxylation and decarbonylation of oleic acid was occurred whereas decarboxylation is the dominating chemical reaction. FTIR results also confirmed the decarboxylation of oleic acid and density measurement of the liquid proves that it falls between the diesel and kerosene. Please click Additional Files below to see the full abstract

Optimizing Hybrid Plate Fixation with a Locked, Oblique End Screw in Osteoporotic Fractures

Background The end screw in a fracture plate creates the greatest resistance to bending. For osteoporotic fractures treated with plates, there is some question as to the optimal screw insertion technique for the screw farthest from the fracture. A locked, oblique end screw was previously shown to increase resistance to periprosthetic fracture. It is unknown, however, how this end screw configuration would resist pullout when subjected to bending. Methods Narrow, low contact 3.5 mm locking compression plates with 6 and 12 holes were anchored to simulated bone material with material properties representing osteoporotic bone. Four configurations were evaluated for the end screw: perpendicular and angulated 30 degrees away from the fracture for both non-locked and locked screws (n=6 per group). The constructs were subjected to 3 point bending until the peak load and finally total construct failure was achieved. Results Peak force, stiffness, energy to peak load, and the failure mode of each construct were determined. All four 12-hole construct groups failed by gross plastic bending deformation of the plate at the fulcrum past a previously established clinically relevant limit for failure (15°). All 12-hole plate constructs failed at statistically higher loads and energy than any of the 6-hole plate constructs, with the exception of the 6-hole locked, oblique construct. Conclusion The locked, oblique end screw provides equivalent pull out strength for 3.5 mm low contact plates regardless of plate length. Combined with its resistance to periprosthetic fracture, this end screw configuration appears to be the best option for the construct integrity of hybrid plating for osteoporotic fractures. Clinical Relevance Osteoporotic fractures are challenging to treat. The current study and the existing literature show that resistance to both bending loads and refracture at the end of a plate are minimized with a locked screw angled away from the fracture

Horizontal DNA transfer mechanisms of bacteria as weapons of intragenomic conflict

Horizontal DNA transfer (HDT) is a pervasive mechanism of diversification in many microbial species, but its primary evolutionary role remains controversial. Much recent research has emphasised the adaptive benefit of acquiring novel DNA, but here we argue instead that intragenomic conflict provides a coherent framework for understanding the evolutionary origins of HDT. To test this hypothesis, we developed a mathematical model of a clonally descended bacterial population undergoing HDT through transmission of mobile genetic elements (MGEs) and genetic transformation. Including the known bias of transformation toward the acquisition of shorter alleles into the model suggested it could be an effective means of counteracting the spread of MGEs. Both constitutive and transient competence for transformation were found to provide an effective defence against parasitic MGEs; transient competence could also be effective at permitting the selective spread of MGEs conferring a benefit on their host bacterium. The coordination of transient competence with cell-cell killing, observed in multiple species, was found to result in synergistic blocking of MGE transmission through releasing genomic DNA for homologous recombination while simultaneously reducing horizontal MGE spread by lowering the local cell density. To evaluate the feasibility of the functions suggested by the modelling analysis, we analysed genomic data from longitudinal sampling of individuals carrying Streptococcus pneumoniae. This revealed the frequent within-host coexistence of clonally descended cells that differed in their MGE infection status, a necessary condition for the proposed mechanism to operate. Additionally, we found multiple examples of MGEs inhibiting transformation through integrative disruption of genes encoding the competence machinery across many species, providing evidence of an ongoing "arms race." Reduced rates of transformation have also been observed in cells infected by MGEs that reduce the concentration of extracellular DNA through secretion of DNases. Simulations predicted that either mechanism of limiting transformation would benefit individual MGEs, but also that this tactic's effectiveness was limited by competition with other MGEs coinfecting the same cell. A further observed behaviour we hypothesised to reduce elimination by transformation was MGE activation when cells become competent. Our model predicted that this response was effective at counteracting transformation independently of competing MGEs. Therefore, this framework is able to explain both common properties of MGEs, and the seemingly paradoxical bacterial behaviours of transformation and cell-cell killing within clonally related populations, as the consequences of intragenomic conflict between self-replicating chromosomes and parasitic MGEs. The antagonistic nature of the different mechanisms of HDT over short timescales means their contribution to bacterial evolution is likely to be substantially greater than previously appreciated

Search for the lepton-flavor-violating decays Bs0→e±μ∓ and B0→e±μ∓

A search for the lepton-flavor-violating decays Bs0→e±μ∓ and B0→e±μ∓ is performed with a data sample, corresponding to an integrated luminosity of 1.0  fb-1 of pp collisions at √s=7  TeV, collected by the LHCb experiment. The observed number of Bs0→e±μ∓ and B0→e±μ∓ candidates is consistent with background expectations. Upper limits on the branching fractions of both decays are determined to be B(Bs0→e±μ∓)101  TeV/c2 and MLQ(B0→e±μ∓)>126  TeV/c2 at 95% C.L., and are a factor of 2 higher than the previous bounds

New genetic loci implicated in fasting glucose homeostasis and their impact on type 2 diabetes risk.

Levels of circulating glucose are tightly regulated. To identify new loci influencing glycemic traits, we performed meta-analyses of 21 genome-wide association studies informative for fasting glucose, fasting insulin and indices of beta-cell function (HOMA-B) and insulin resistance (HOMA-IR) in up to 46,186 nondiabetic participants. Follow-up of 25 loci in up to 76,558 additional subjects identified 16 loci associated with fasting glucose and HOMA-B and two loci associated with fasting insulin and HOMA-IR. These include nine loci newly associated with fasting glucose (in or near ADCY5, MADD, ADRA2A, CRY2, FADS1, GLIS3, SLC2A2, PROX1 and C2CD4B) and one influencing fasting insulin and HOMA-IR (near IGF1). We also demonstrated association of ADCY5, PROX1, GCK, GCKR and DGKB-TMEM195 with type 2 diabetes. Within these loci, likely biological candidate genes influence signal transduction, cell proliferation, development, glucose-sensing and circadian regulation. Our results demonstrate that genetic studies of glycemic traits can identify type 2 diabetes risk loci, as well as loci containing gene variants that are associated with a modest elevation in glucose levels but are not associated with overt diabetes

Building Babies - Chapter 16

In contrast to birds, male mammals rarely help to raise the offspring. Of all mammals, only among rodents, carnivores, and primates, males are sometimes intensively engaged in providing infant care (Kleiman and Malcolm 1981). Male caretaking of infants has long been recognized in nonhuman primates (Itani 1959). Given that infant care behavior can have a positive effect on the infant’s development, growth, well-being, or survival, why are male mammals not more frequently involved in “building babies”? We begin the chapter defining a few relevant terms and introducing the theory and hypotheses that have historically addressed the evolution of paternal care. We then review empirical findings on male care among primate taxa, before focusing, in the final section, on our own work on paternal care in South American owl monkeys (Aotus spp.). We conclude the chapter with some suggestions for future studies.Deutsche Forschungsgemeinschaft (HU 1746/2-1) Wenner-Gren Foundation, the L.S.B. Leakey Foundation, the National Geographic Society, the National Science Foundation (BCS-0621020), the University of Pennsylvania Research Foundation, the Zoological Society of San Dieg

Genome-wide trans-ancestry meta-analysis provides insight into the genetic architecture of type 2 diabetes susceptibility.

To further understanding of the genetic basis of type 2 diabetes (T2D) susceptibility, we aggregated published meta-analyses of genome-wide association studies (GWAS), including 26,488 cases and 83,964 controls of European, east Asian, south Asian and Mexican and Mexican American ancestry. We observed a significant excess in the directional consistency of T2D risk alleles across ancestry groups, even at SNPs demonstrating only weak evidence of association. By following up the strongest signals of association from the trans-ethnic meta-analysis in an additional 21,491 cases and 55,647 controls of European ancestry, we identified seven new T2D susceptibility loci. Furthermore, we observed considerable improvements in the fine-mapping resolution of common variant association signals at several T2D susceptibility loci. These observations highlight the benefits of trans-ethnic GWAS for the discovery and characterization of complex trait loci and emphasize an exciting opportunity to extend insight into the genetic architecture and pathogenesis of human diseases across populations of diverse ancestry