Design method and performance comparison of plenum and volute delivery systems for radial inflow turbines

Radial inflow turbines are the preferred architecture for energy extraction from the organic Rankine cycle and the supercritical CO Brayton cycle at smaller scales. For such turbines it is possible for fluid to be delivered to the first stage by either a volute or plenum delivery system. For high pressure supercritical CO turbines, there are no fully documented fluid delivery systems in literature and it remains unclear as to which architecture results in higher performance with the highly dense working fluid. The aim of this paper is to present a performance comparison between a new plenum based fluid delivery system and conventional volute for a 100 kW supercritical CO radial inflow turbine. Numerical simulations of the fluid delivery systems are conducted and compared in terms of flow uniformity, total pressure loss and entropy rise. It is demonstrated that fluid can be delivered to the stator vanes with a plenum style inlet for a radial inflow supercritical CO turbine without re-circulation regions and minimal total pressure loss. Entropy rise for the plenum is reduced more than tenfold in comparison to the volute, however fluid velocities are not matched and there is a periodic variation in in velocity generated by the multiple inlets

Tectonics and volcanism of Eastern Aphrodite Terra: No subduction, no spreading

Eastern Aphrodite Terra is approximately equal in size to the western North American Cordillera, from Mexico to Alaska. Its size and unique landforms make it an important area for understanding the tectonics of Venus, yet models for its formation are diametrically opposed. This region is part of the Equatorial Highlands, which was proposed as a region of lithospheric thinning, isostatic uplift, and attendant volcanism. Eastern Aphrodite Terra is dominated by circular structures within which deformation and volcanism are intimately related. These structures are marked by radial and concentric fractures, and volcanic flows that emanate from a central vent, as well as from concentric fracture sets. Cross-cutting relations between flows and concentric fracture sets indicate that outer concentric fracture sets are younger than inner fracture sets. The circular structures are joined by regional northeast- to east-trending fractures that dominantly postdate formation of the circular structures. We propose that the circular structures 'grow' outward with time. Although these structures probably represent addition of crust to the lithosphere, they do not represent significant lithospheric spreading or convergence, and the region does not mark the boundary between two distinct tectonic plates. This region is not easily explained by analogy with either terrestrial midocean rifts or subduction zones. It is perhaps best explained by upwelling of magma diapirs that blister the surface, but do not cause significant lithospheric spreading. Further study of the structural and volcanic evolution of this region using Magellan altimetry and SAR data should lead to better understanding of the tectonic evolution of this region

Dbl3 drives Cdc42 signaling at the apical margin to regulate junction position and apical differentiation

Epithelial cells develop morphologically characteristic apical domains that are bordered by tight junctions, the apical–lateral border. Cdc42 and its effector complex Par6–atypical protein kinase c (aPKC) regulate multiple steps during epithelial differentiation, but the mechanisms that mediate process-specific activation of Cdc42 to drive apical morphogenesis and activate the transition from junction formation to apical differentiation are poorly understood. Using a small interfering RNA screen, we identify Dbl3 as a guanine nucleotide exchange factor that is recruited by ezrin to the apical membrane, that is enriched at a marginal zone apical to tight junctions, and that drives spatially restricted Cdc42 activation, promoting apical differentiation. Dbl3 depletion did not affect junction formation but did affect epithelial morphogenesis and brush border formation. Conversely, expression of active Dbl3 drove process-specific activation of the Par6–aPKC pathway, stimulating the transition from junction formation to apical differentiation and domain expansion, as well as the positioning of tight junctions. Thus, Dbl3 drives Cdc42 signaling at the apical margin to regulate morphogenesis, apical–lateral border positioning, and apical differentiation

RpfC (Rv1884) atomic structure shows high structural conservation within the resuscitation promoting factor catalytic domain

We report the first structure of the catalytic domain of RpfC (Rv1884), one of theresuscitation-promoting factors (RPFs) from Mycobacterium tuberculosis. The structure was solved using molecular replacement, once the space group had been correctly identified as twinned P21 rather than the apparent C2221 by searching for anomalous scattering sites in P1. The structure displays a very high degree of structural conservation with the structures of the catalytic domains of RpfB (Rv1009) and RpfE (Rv2450) already published. This structural conservation highlights the importance of the versatile domain composition of the RPF family

Cell wall peptidoglycan in Mycobacterium tuberculosis: An Achilles’ heel for the TB-causing pathogen

Tuberculosis (TB), caused by the intracellular pathogen Mycobacterium tuberculosis, remains one of the leading causes of mortality across the world. There is an urgent requirement to build a robust arsenal of effective antimicrobials, targeting novel molecular mechanisms to overcome the challenges posed by the increase of antibiotic resistance in TB. Mycobacterium tuberculosis has a unique cell envelope structure and composition, containing a peptidoglycan layer that is essential for maintaining cellular integrity and for virulence. The enzymes involved in the biosynthesis, degradation, remodelling and recycling of peptidoglycan have resurfaced as attractive targets for anti-infective drug discovery. Here, we review the importance of peptidoglycan, including the structure, function and regulation of key enzymes involved in its metabolism. We also discuss known inhibitors of ATP-dependent Mur ligases, and discuss the potential for the development of pan-enzyme inhibitors targeting multiple Mur ligases

Helicobacter pylori phagosome maturation in primary human macrophages

Extent: 14p.Background: Helicobacter pylori (H. pylori) is a micro-aerophilic, spiral-shaped, motile bacterium that is the principal cause of gastric and duodenal ulcers in humans and is a major risk factor for the development of gastric cancer. Despite provoking a strong innate and adaptive immune response in the host, H. pylori persists in the gastric mucosa, avoiding eradication by macrophages and other phagocytic cells, which are recruited to the site of infection. Here we have characterised the critical degradative process of phagosome maturation in primary human macrophages for five genotypically and phenotypically distinct clinical strains of H. pylori. Results: All of the H. pylori strains examined showed some disruption to the phagosome maturation process, when compared to control E. coli. The early endosome marker EEA1 and late endosome marker Rab7 were retained on H. pylori phagosomes, while the late endosome-lysosome markers CD63, LAMP-1 and LAMP-2 were acquired in an apparently normal manner. Acquisition of EEA1 by H. pylori phagosomes appeared to occur by two distinct, strain specific modes. H. pylori strains that were negative for the cancer associated virulence factor CagA were detected in phagosomes that recruited large amounts of EEA1 relative to Rab5, compared to CagA positive strains. There were also strain specific differences in the timing of Rab7 acquisition which correlated with differences in the rate of intracellular trafficking of phagosomes and the timing of megasome formation. Megasomes were observed for all of the H. pylori strains examined. Conclusions: H. pylori appeared to disrupt the normal process of phagosome maturation in primary human macrophages, appearing to block endosome fission. This resulted in the formation of a hybrid phagosome-endosome-lysosome compartment, which we propose has reduced degradative capacity. Reduced killing by phagocytes is consistent with the persistence of H. pylori in the host, and would contribute to the chronic stimulation of the inflammatory immune response, which underlies H. pylori-associated disease.Glenn N Borlace, Hilary F Jones, Stacey J Keep, Ross N Butler, Doug A Brook