Air Entrainment Processes in a Full-Scale Rectangular Dropshaft at Large Flows

Rectangular dropshafts, commonly used in sewers and storm water systems, are characterised by significant flow aeration. New detailed air-water flow measurements were conducted in a near-full-scale dropshaft at large discharges. In the shaft pool and outflow channel, the results demonstrated the complexity of different competitive air entrainment mechanisms. Bubble size measurements showed a broad range of entrained bubble sizes. Analysis of streamwise distributions of bubbles suggested further some clustering process in the bubbly flow although, in the outflow channel, bubble chords were in average smaller than in the shaft pool. A robust hydrophone was tested to measure bubble acoustic spectra and to assess its field application potential. The acoustic results characterised accurately the order of magnitude of entrained bubble sizes, but the transformation from acoustic frequencies to bubble radii did not predict correctly the probability distribution functions of bubble sizes.

Kostean höyryn paisunnan erityispiirteet ydinvoimalaitosten turbiineissa

Diplomityössä käsitellään ydinvoimalaitoksen kostean höyryn alueella toimivien höyryturbiinien toiminnan erityispiirteitä. Tarkemmin työssä keskitytään Loviisan ydinvoimalaitoksen turbiiniprosessiin. Tavoitteena on selvittää veden tiivistymistä höyryvirrassa, sen erotusta höyrystä turbiineissa sekä määrittää laitokselle todellinen paisuntakäyrä. Työssä selvitettiin veden tiivistymistä höyryvirtaan kirjallisuuden ja prosessista saatujen tietojen perusteella. Lisäksi työssä tutustuttiin suurien nykyaikaisten kostean höyryn alueella toimivien turbiinien vedenerotukseen ja sen pohjalta arvioitiin Loviisan ydinvoimalaitoksen turbiinin kosteudenerotusta. Näiden tietojen avulla saatiin mallinnettua kostean höyryn paisuntakäyrä Loviisan ydinvoimalaitoksen turbiineille. Työssä perehdyttiin lisäksi ulosvirtauskanavan toimintaan. Diplomityön puitteissa ei perehdytty yksityiskohtaisesti veden tiivistymiseen höyryvirrassa, vaan aihe ansaitsee tarkempaa tutkimusta. Kosteuden erotustehokkuuden arviointi todellisessa prosessissa ilman mittauksista saatavaa tietoa on vaikeata, mutta toimenpiteisiin lisäinformaation saamiseksi Loviisan ydinvoimalaitoksen turbiiniprosessista on ryhdytty. Työssä tehtyjen selvitysten avulla saatiin arvokasta tietoa turbiinikoneikon toiminnasta ja sen tehokkuuden parantamisesta.

Exogenous vascular endothelial growth factor induces malformed and hyperfused vessels during embryonic neovascularization.

Vascular endothelial growth factor (VEGF) is a potent and specific endothelial mitogen that is able to induce angiogenesis in vivo [Leung, D. W., Cachianes, G., Kuang, W.-J., Goeddel, D. V. & Ferrara, N. (1989) Science 246 1306-1309]. To determine if VEGF also influences the behavior of primordial endothelial cells, we used an in vivo vascular assay based on the de novo formation of vessels. Japanese quail embryos injected with nanomolar quantities of the 165-residue form of VEGF at the onset of vasculogenesis exhibited profoundly altered vessel development. In fact, the overall patterning of the vascular network was abnormal in all VEGF-injected embryos. The malformations were attributable to two specific endothelial cell activities: (i) inappropriate neovascularization in normally avascular areas and (ii) the unregulated, excessive fusion of vessels. In the first instance, supernumerary vessels directly linked the inflow channel of the heart to the aortic outflow channel. The second aberrant activity led to the formation of vessels with abnormally large lumens. Ultimately, unregulated vessel fusion generated massive vascular sacs that obliterated the identity of individual vessels. These observations show that exogenous VEGF has an impact on the behavior of primordial endothelial cells engaged in vasculogenesis, and they strongly suggest that endogenous VEGF is important in vascular patterning and regulation of vessel size (lumen formation).

THE IMPACT OF UPPER-LEVEL PROCESSES ON THE INTENSITY AND STRUCTURAL CHANGES OF HURRICANE SANDY (2012)

The first part of this study examines the relative roles of frontogenesis and tropopause undulation in determining the intensity and structural changes of Hurricane Sandy (2012) using a high-resolution cloud-resolving model. A 138-h simulation reproduces Sandy’s four distinct development stages: (i) rapid intensification, (ii) weakening, (iii) steady maximum surface wind but with large continued sea-level pressure (SLP) falls, and (iv) re-intensification. Results show typical correlations between intensity changes, sea-surface temperature and vertical wind shear during the first two stages. The large SLP falls during the last two stages are mostly caused by Sandy’s moving northward into lower-tropopause regions associated with an eastward-propagating midlatitude trough, where the associated lower-stratospheric warm air wraps into the storm and its surrounding areas. The steady maximum surface wind occurs because of the widespread SLP falls with weak pressure gradients lacking significant inward advection of absolute angular momentum (AAM). Meanwhile, there is a continuous frontogenesis in the outer region during the last three stages. Cyclonic inward advection of AAM along each frontal rainband accounts for the continued expansion of the tropical-storm-force wind and structural changes, while deep convection in the eyewall and merging of the final two survived frontal rainbands generate a spiraling jet in Sandy’s northwestern quadrant, leading to its re-intensification prior to landfall. The physical, kinematic and dynamic aspects of an upper-level outflow layer and its possible impact on the re-intensification of Sandy are examined in the second part of this study. Above the outflow layer isentropes are tilted downward with radius as a result of the development of deep convection and an approaching upper-level trough, causing weak subsidence. Its maximum outward radial velocity is located above the cloud top, so the outflow channel experiences cloud-induced long-wave cooling. Because Sandy has two distinct convective regions (an eyewall and a frontal rainband), it has multiple outflow layers, with the eyewall’s outflow layer located above that of the frontal rainband. During the re-intensification stage, the eyewall’s outflow layer interacts with a jet stream ahead of the upper-level trough axis. Because of the presence of inertial instability on the anticyclonic side of the jet stream and symmetric instability in the inner region of the outflow layer, Sandy’s secondary circulation intensifies. Its re-intensification ceases when these instabilities disappear. The relationship between the intensity of the secondary circulation and dynamic instabilities of the outflow layer suggests that the re-intensification occurs in response to these instabilities. Additionally, it is verified that the long-wave cooling in the outflow layer helps induce symmetric instability by reducing static stability.

Specific inhibition of HCN channels slows rhythm differently in atria, ventricle and outflow tract and stabilizes conduction in the anoxic-reoxygenated embryonic heart model.

The hyperpolarization-activated cyclic nucleotide-gated (HCN) channels are expressed in pacemaker cells very early during cardiogenesis. This work aimed at determining to what extent these channels are implicated in the electromechanical disturbances induced by a transient oxygen lack which may occur in utero. Spontaneously beating hearts or isolated ventricles and outflow tracts dissected from 4-day-old chick embryos were exposed to a selective inhibitor of HCN channels (ivabradine 0.1-10microM) to establish a dose-response relationship. The effects of ivabradine on electrocardiogram, excitation-contraction coupling and contractility of hearts submitted to anoxia (30min) and reoxygenation (60min) were also determined. The distribution of the predominant channel isoform, HCN4, was established in atria, ventricle and outflow tract by immunoblotting. Intrinsic beating rate of atria, ventricle and outflow tract was 164+/-22 (n=10), 78+/-24 (n=8) and 40+/-12bpm (n=23, mean+/-SD), respectively. In the whole heart, ivabradine (0.3microM) slowed the firing rate of atria by 16% and stabilized PR interval. These effects persisted throughout anoxia-reoxygenation, whereas the variations of QT duration, excitation-contraction coupling and contractility, as well as the types and duration of arrhythmias were not altered. Ivabradine (10microM) reduced the intrinsic rate of atria and isolated ventricle by 27% and 52%, respectively, whereas it abolished activity of the isolated outflow tract. Protein expression of HCN4 channels was higher in atria and ventricle than in the outflow tract. Thus, HCN channels are specifically distributed and control finely atrial, ventricular and outflow tract pacemakers as well as conduction in the embryonic heart under normoxia and throughout anoxia-reoxygenation.

Ferromanganese nodules and micro-hardgrounds associated with the Cadiz Contourite Channel (NE Atlantic): Palaeoenvironmental records of fluid venting and bottom currents

Ferromanganese nodule fields and hardgrounds have recently been discovered in the Cadiz Contourite Channel in the Gulf of Cadiz (850–1000 m). This channel is part of a large contourite depositional system generated by the Mediterranean Outflow Water. Ferromanganese deposits linked to contourites are interesting tools for palaeoenviromental studies and show an increasing economic interest as potential mineral resources for base and strategic metals. We present a complete characterisation of these deposits based on submarine photographs and geophysical, petrographic, mineralogical and geochemical data. The genesis and growth of ferromanganese deposits, strongly enriched in Fe vs. Mn (av. 39% vs. 6%) in this contourite depositional system result from the combination of hydrogenetic and diagenetic processes. The interaction of the Mediterranean Outflow Water with the continental margin has led to the formation of Late Pleistocene–Holocene ferromanganese mineral deposits, in parallel to the evolution of the contourite depositional system triggered by climatic and tectonic events. The diagenetic growth was fuelled by the anaerobic oxidation of thermogenic hydrocarbons (δ13CPDB=−20 to −37‰) and organic matter within the channel floor sediments, promoting the formation of Fe–Mn carbonate nodules. High 87Sr/86Sr isotopic values (up to 0.70993±0.00025) observed in the inner parts of nodules are related to the influence of radiogenic fluids fuelled by deep-seated fluid venting across the fault systems in the diapirs below the Cadiz Contourite Channel. Erosive action of the Mediterranean Outflow Water undercurrent could have exhumed the Fe–Mn carbonate nodules, especially in the glacial periods, when the lower core of the undercurrent was more active in the study area. The growth rate determined by 230Thexcess/232Th was 113±11 mm/Ma, supporting the hypothesis that the growth of the nodules records palaeoenvironmental changes during the last 70 ka. Ca-rich layers in the nodules could point to the interaction between the Mediterranean Outflow Water and the North Atlantic Deep Water during the Heinrich events. Siderite–rhodochrosite nodules exposed to the oxidising seabottom waters were replaced by Fe–Mn oxyhydroxides. Slow hydrogenetic growth of goethite from the seawaters is observed in the outermost parts of the exhumed nodules and hardgrounds, which show imprints of the Mediterranean Outflow Water with low 87Sr/86Sr isotopic values (down to 0.70693±0.00081). We propose a new genetic and evolutionary model for ferromanganese oxide nodules derived from ferromanganese carbonate nodules formed on continental margins above the carbonate compensation depth and dominated by hydrocarbon seepage structures and strong erosive action of bottom currents. We also compare and discuss the generation of ferromanganese deposits in the Cadiz Contourite Channel with that in other locations and suggest that our model can be applied to ferromanganiferous deposits in other contouritic systems affected by fluid venting.

Changes In The Bacterial Community Of Soil From A Neutral Mine Drainage Channel.

Mine drainage is an important environmental disturbance that affects the chemical and biological components in natural resources. However, little is known about the effects of neutral mine drainage on the soil bacteria community. Here, a high-throughput 16S rDNA pyrosequencing approach was used to evaluate differences in composition, structure, and diversity of bacteria communities in samples from a neutral drainage channel, and soil next to the channel, at the Sossego copper mine in Brazil. Advanced statistical analyses were used to explore the relationships between the biological and chemical data. The results showed that the neutral mine drainage caused changes in the composition and structure of the microbial community, but not in its diversity. The Deinococcus/Thermus phylum, especially the Meiothermus genus, was in large part responsible for the differences between the communities, and was positively associated with the presence of copper and other heavy metals in the environmental samples. Other important parameters that influenced the bacterial diversity and composition were the elements potassium, sodium, nickel, and zinc, as well as pH. The findings contribute to the understanding of bacterial diversity in soils impacted by neutral mine drainage, and demonstrate that heavy metals play an important role in shaping the microbial population in mine environments.

Taurine Supplementation Increases K(atp) Channel Protein Content, Improving Ca2+ Handling And Insulin Secretion In Islets From Malnourished Mice Fed On A High-fat Diet.

Pancreatic β-cells are highly sensitive to suboptimal or excess nutrients, as occurs in protein-malnutrition and obesity. Taurine (Tau) improves insulin secretion in response to nutrients and depolarizing agents. Here, we assessed the expression and function of Cav and KATP channels in islets from malnourished mice fed on a high-fat diet (HFD) and supplemented with Tau. Weaned mice received a normal (C) or a low-protein diet (R) for 6 weeks. Half of each group were fed a HFD for 8 weeks without (CH, RH) or with 5% Tau since weaning (CHT, RHT). Isolated islets from R mice showed lower insulin release with glucose and depolarizing stimuli. In CH islets, insulin secretion was increased and this was associated with enhanced KATP inhibition and Cav activity. RH islets secreted less insulin at high K(+) concentration and showed enhanced KATP activity. Tau supplementation normalized K(+)-induced secretion and enhanced glucose-induced Ca(2+) influx in RHT islets. R islets presented lower Ca(2+) influx in response to tolbutamide, and higher protein content and activity of the Kir6.2 subunit of the KATP. Tau increased the protein content of the α1.2 subunit of the Cav channels and the SNARE proteins SNAP-25 and Synt-1 in CHT islets, whereas in RHT, Kir6.2 and Synt-1 proteins were increased. In conclusion, impaired islet function in R islets is related to higher content and activity of the KATP channels. Tau treatment enhanced RHT islet secretory capacity by improving the protein expression and inhibition of the KATP channels and enhancing Synt-1 islet content.

The Analgesic Effect Of Dipyrone In Peripheral Tissue Involves Two Different Mechanisms: Neuronal K(atp) Channel Opening And Cb(1) Receptor Activation.

Dipyrone (metamizole) is an analgesic pro-drug used to control moderate pain. It is metabolized in two major bioactive metabolites: 4-methylaminoantipyrine (4-MAA) and 4-aminoantipyrine (4-AA). The aim of this study was to investigate the participation of peripheral CB1 and CB2 cannabinoid receptors activation in the anti-hyperalgesic effect of dipyrone, 4-MAA or 4-AA. PGE2 (100ng/50µL/paw) was locally administered in the hindpaw of male Wistar rats, and the mechanical nociceptive threshold was quantified by electronic von Frey test, before and 3h after its injection. Dipyrone, 4-MAA or 4-AA was administered 30min before the von Frey test. The selective CB1 receptor antagonist AM251, CB2 receptor antagonist AM630, cGMP inhibitor ODQ or KATP channel blocker glibenclamide were administered 30min before dipyrone, 4-MAA or 4-AA. The antisense-ODN against CB1 receptor expression was intrathecally administered once a day during four consecutive days. PGE2-induced mechanical hyperalgesia was inhibited by dipyrone, 4-MAA, and 4-AA in a dose-response manner. AM251 or ODN anti-sense against neuronal CB1 receptor, but not AM630, reversed the anti-hyperalgesic effect mediated by 4-AA, but not by dipyrone or 4-MAA. On the other hand, the anti-hyperalgesic effect of dipyrone or 4-MAA was reversed by glibenclamide or ODQ. These results suggest that the activation of neuronal CB1, but not CB2 receptor, in peripheral tissue is involved in the anti-hyperalgesic effect of 4-aminoantipyrine. In addition, 4-methylaminoantipyrine mediates the anti-hyperalgesic effect by cGMP activation and KATP opening.

Outflow occlusion for circulatory arrest in dogs

The purpose of this study was to evaluate the possibility of producing circulatory arrest by occlusion of the pulmonary trunk as an alternative to the venous inflow occlusion through the left hemithorax. Eight healthy mongrel dogs were divided in two groups. Group I underwent 4 minutes of outflow occlusion and Group II was submitted to 8 minutes of circulatory arrest. Outflow occlusion was performed through left thoracotomy and pericardiotomy by passing a Rumel tourniquet around the pulmonary trunk. Physical examination, electrocardiography, echocardiography, blood gas analyses, hemodynamic, and oxygen transport variables were obtained before and after the procedure. The dogs from Group I did not have any clinical, electrocardiographic, echocardiographic, or hemo-dynamic abnormalities after anesthetic recover. In the Group II, only one dog survived, which had no clinical, electrocardiographic, or echocardiographic abnormalities. In this last dog, just after releasing the occlusion, it was detected increases in the following parameters: heart rate (HR), systolic, diastolic and mean arterial blood pressure (SAP; DAP; MAP), pulmonary artery pressure (PAP), pulmonary wedge pressure (PWP), central venous pressure (CVP), cardiac output (CO), systolic index (SI), cardiac index (CI), left and right ventricular stroke work (LVSW; RVSW), oxygen delivery index (DO2), oxygen consumption index (VO2), and oxygen extraction (O2 ext). Moreover, the oxygen content of arterial and mixed venous blood (CaO2; CvO2), and the arterial and mixed venous partial pressure of oxygen (PaO2; PvO2) were decreased 5 minutes after circulatory arrest. Outflow occlusion is a feasible surgical procedure for period of 4 minutes of circulatory arrest.

Allosteric Control of Gating Mechanisms Revisited: The Large Conductance Ca(2+)-Activated K(+) Channel

Large-conductance Ca(2+)-activated K(+) channels (BK) play a fundamental role in modulating membrane potential in many cell types. The gating of BK channels and its modulation by Ca(2+) and voltage has been the subject of intensive research over almost three decades, yielding several of the most complicated kinetic mechanisms ever proposed. A large number of open and closed states disposed, respectively, in two planes, named tiers, characterize these mechanisms. Transitions between states in the same plane are cooperative and modulated by Ca(2+). Transitions across planes are highly concerted and voltage-dependent. Here we reexamine the validity of the two-tiered hypothesis by restricting attention to the modulation by Ca(2+). Large single channel data sets at five Ca(2+) concentrations were simultaneously analyzed from a Bayesian perspective by using hidden Markov models and Markov-chain Monte Carlo stochastic integration techniques. Our results support a dramatic reduction in model complexity, favoring a simple mechanism derived from the Monod-Wyman-Changeux allosteric model for homotetramers, able to explain the Ca(2+) modulation of the gating process. This model differs from the standard Monod-Wyman-Changeux scheme in that one distinguishes when two Ca(2+) ions are bound to adjacent or diagonal subunits of the tetramer.

Chaotic model and memory in single calcium-activated potassium channel kinetics

Ion channels are pores formed by proteins and responsible for carrying ion fluxes through cellular membranes. The ion channels can assume conformational states thereby controlling ion flow. Physically, the conformational transitions from one state to another are associated with energy barriers between them and are dependent on stimulus, such as, electrical field, ligands, second messengers, etc. Several models have been proposed to describe the kinetics of ion channels. The classical Markovian model assumes that a future transition is independent of the time that the ion channel stayed in a previous state. Others models as the fractal and the chaotic assume that the rate of transitions between the states depend on the time that the ionic channel stayed in a previous state. For the calcium activated potassium channels of Leydig cells the R/S Hurst analysis has indicated that the channels are long-term correlated with a Hurst coefficient H around 0.7, showing a persistent memory in this kinetic. Here, we applied the R/S analysis to the opening and closing dwell time series obtained from simulated data from a chaotic model proposed by L. Liebovitch and T. Toth [J. Theor. Biol. 148, 243 (1991)] and we show that this chaotic model or any model that treats the set of channel openings and closings as independent events is inadequate to describe the long-term correlation (memory) already described for the experimental data. (C) 2008 American Institute of Physics.

Expression of an activating mutation in the gene encoding the K(ATP) channel subunit Kir6.2 in mouse pancreatic beta cells recapitulates neonatal diabetes

Neonatal diabetes is a rare monogenic form of diabetes that usually presents within the first six months of life. It is commonly caused by gain-of-function mutations in the genes encoding the Kir6.2 and SUR1 subunits of the plasmalemmal ATP-sensitive K(+) (K(ATP)) channel. To better understand this disease, we generated a mouse expressing a Kir6.2 mutation (V59M) that causes neonatal diabetes in humans and we used Cre-lox technology to express the mutation specifically in pancreatic beta cells. These beta-V59M mice developed severe diabetes soon after birth, and by 5 weeks of age, blood glucose levels were markedly increased and insulin was undetectable. Islets isolated from beta-V59M mice secreted substantially less insulin and showed a smaller increase in intracellular calcium in response to glucose. This was due to a reduced sensitivity of K(ATP) channels in pancreatic beta cells to inhibition by ATP or glucose. In contrast, the sulfonylurea tolbutamide, a specific blocker of K(ATP) channels, closed K(ATP) channels, elevated intracellular calcium levels, and stimulated insulin release in beta-V59M beta cells, indicating that events downstream of K(ATP) channel closure remained intact. Expression of the V59M Kir6.2 mutation in pancreatic beta cells alone is thus sufficient to recapitulate the neonatal diabetes observed in humans. beta-V59M islets also displayed a reduced percentage of beta cells, abnormal morphology, lower insulin content, and decreased expression of Kir6.2, SUR1, and insulin mRNA. All these changes are expected to contribute to the diabetes of beta-V59M mice. Their cause requires further investigation.

Potent Cardioprotective Effect of the 4-Anilinoquinazoline Derivative PD153035: Involvement of Mitochondrial K(ATP) Channel Activation

Background: The aim of the present study was to evaluate the protective effects of the 4-anilinoquinazoline derivative PD153035 on cardiac ischemia/reperfusion and mitochondrial function. Methodology/Principal Findings: Perfused rat hearts and cardiac HL-1 cells were used to determine cardioprotective effects of PD153035. Isolated rat heart mitochondria were studied to uncover mechanisms of cardioprotection. Nanomolar doses of PD153035 strongly protect against heart and cardiomyocyte damage induced by ischemia/reperfusion and cyanide/aglycemia. PD153035 did not alter oxidative phosphorylation, nor directly prevent Ca(2+) induced mitochondrial membrane permeability transition. The protective effect of PD153035 on HL-1 cells was also independent of AKT phosphorylation state. Interestingly, PD153035 activated K(+) transport in isolated mitochondria, in a manner prevented by ATP and 5-hydroxydecanoate, inhibitors of mitochondrial ATP-sensitive K(+) channels (mitoK(ATP)). 5-Hydroxydecanoate also inhibited the cardioprotective effect of PD153035 in cardiac HL-1 cells, demonstrating that this protection is dependent on mitoK(ATP) activation. Conclusions/Significance: We conclude that PD153035 is a potent cardioprotective compound and acts in a mechanism involving mitoK(ATP) activation.