Elevating Pressure Research Articles

Сombustion of Micro- and Nanothermites under Elevating Pressure

Non-equilibrium process of combustion-wave propagation of thermite compositions (Mg/Fe2O3) inside the sealed steel tube have been investigated to study the burning rate at elevating pressure. Under confinement the hot gas-phase products, formed during thermite combustion result in considerable overpressure inside the tube that reverses the gas flow and leads to pressure-driven preheating effect of the burned-gas permeation. Convective origin of this preheating effect is discussed. The pressure-time dependency is obtained experimentally. The composition was pressed inside the steel tube in pellets; the size of each part was measured to obtain burning rate – pressure dependency. Both micro- and nanosized components were used to prepare thermite compositions under study. The significant difference in burning parameters of micron- and nanosized thermites is observed and analyzed. Based on obtained results, the combustion mechanism of thermites with the micro- and nanosized components is discussed.

Numerical Simulations of Flat Laminar Premixed Methane-Air Flames at Elevated Pressure

Two-dimensional axisymmetric simulation of stoichiometric methane-air flames stabilized on flat burners at elevated pressure is reported in the present work. Such flames, in practice, are experimentally obtained using the heat flux method for measurement of laminar burning velocity of fuel-oxidizer mixtures (Bosschaart and de Goey, 2004; Goswami et al., 2013). The method makes use of a burner with a perforated brass burner plate. The dimensions of such a plate play an important role in creating flat flames. The present investigation is focused on studying laminar premixed flame structure numerically at elevated pressure up to 15 bar using a one-step and a detailed chemical reaction mechanism. Three burner plate models (of varying hole diameter and porosity) are used in the simulations for pressures up to 7 bar with a one-step mechanism. The surface area increase of the flame was evaluated based on an isotherm at 900 K and the net reaction rate of methane compared to a flat flame. The comparison of these models shows that the surface area increase can significantly be reduced by choosing a smaller hole diameter and larger porosity. The results of the detailed simulations using an appropriate chemical reaction mechanism up to 15 bar using a burner plate model, which is similar to the ones used in experiments (mentioned above), show a nonlinear increase of the flame curvature with elevating pressure. A hole diameter of 0.25 mm and a pitch of 0.29 mm is suggested for a burner plate in such experiments. Flame structure at elevated pressure is also analyzed further based on species profiles obtained.

Effects of High-Pressure Processing on the Cooking Loss and Gel Strength of Chicken Breast Actomyosin Containing Sodium Alginate

The effects of high-pressure processing (HPP) (0–400 MPa for 10 min) on the cooking loss (CL), gel strength, and thermal gelling mechanism of chicken breast actomyosin solution containing 0.5 % (w/v) sodium alginate (AS-SA) were investigated. The results showed that HPP could significantly increase (P < 0.05) the reactive sulfhydryl contents, surface hydrophobicity, and turbidity of the pressurized sample under 200–400 MPa and gradually decrease its thermal gelling ability with an elevating pressure from 100 to 400 MPa. The HPP under 300 MPa for 10 min could enhance the thermal stability of AS-SA and promote the formation of AS-SA gel structure with large pores and thick strands. Those resulted in the increased gel strength and the increased CL of pressurized AS-SA, which were relative to hydrophobic interaction and disulfide bonding. The information could offer certain theoretical foundation to apply HPP technology for developing meat-SA gels with various properties via combinational use of different HPP levels and SA.

Sorption and Diffusion Behavior of Carbon Dioxide into Poly(l-lactic acid) Films at Elevated Pressures

Equilibrium sorption amount, desorption diffusion coefficients and sorption diffusion coefficients of CO2 in poly(l-lactic acid) (PLLA) films at elevated pressures were determined by the gravimetric method, in which the Fick's diffusion model was applied to analyze both the desorption and sorption processes. The equilibrium sorption amount of CO2 in PLLA increased with lowering temperature and elevating pressure at the temperature range from 40 to 60 °C and pressure from 104 to 2×104 kPa. Desorption diffusion coefficients were greatly influenced by the equilibrium sorption amount, and they were in the same order of magnitude as the sorption diffusion coefficients. The scan electron microscope (SEM) photos demonstrated that there was no foaming phenomenon of the PLLA film during desorption and sorption processes. The XRD spectra implied that the crystalline degree of PLLA film decreased after CO2 processing. It was concluded that PLLA polymer could be well swollen and plasticized by supercritical CO2.

Elevated pressure selectively blunts flow‐evoked vasodilatation in rat mesenteric small arteries

The present study investigated mechanisms underlying impaired endothelium-dependent vasodilatation elicited by elevating the intraluminal pressure in rat mesenteric small arteries. Arterial segments (internal diameter 316+/-2 microm, n=86) were mounted in a pressure myograph. The effect of elevating pressure from 50 to 120 mmHg for 1 h before resetting it to 50 mmHg was studied on endothelium-dependent vasodilatation. In arteries constricted with U46619 in the presence of indomethacin, shear stress generated by flow, evoked vasodilatation that was abolished by an inhibitor of nitric oxide (NO) synthase, asymmetric dimethylarginine (1 mM), whereas acetylcholine-induced vasodilatation was unchanged. After elevation of intraluminal pressure for 1 h and then resetting it to 50 mmHg, vasodilatation induced by shear stress and the NO donor, S-nitrosopenicillamine was inhibited, while vasodilatation induced by a guanylyl cyclase activator, BAY 412272, and acetylcholine was unaltered. Superoxide levels sensitive to polyethylene glycol superoxide dismutase were increased in segments exposed to elevated pressure. A superoxide scavenger, tempol (300 microM), a general endothelin receptor antagonist, SB 217242 and the selective ET(A) receptor antagonist, BQ 123 preserved shear stress-evoked vasodilatation. The present study shows that transient exposure to an elevated intraluminal pressure selectively inhibits flow-evoked NO-mediated vasodilatation, probably through activation of endothelin receptors and increased formation of superoxide. In contrast, elevation of pressure did not affect the acetylcholine-evoked endothelium-derived hyperpolarizing factor type vasodilatation in mesenteric small arteries.

Primary and secondary relaxations in supercooled eugenol and isoeugenol at ambient and elevated pressures: Dependence on chemical microstructure

Dielectric loss spectra of two glass-forming isomers, eugenol and isoeugenol, measured at ambient and elevated pressures in the normal liquid, supercooled, and glassy states are presented. The isomeric chemical compounds studied differ only by the location of the double bond in the alkyl chain. Above the glass transition temperature T(g), the dielectric loss spectra of both isomers exhibit an excess wing on the high frequency flank of the loss peak of the alpha relaxation and an additional faster gamma process at the megahertz frequency range. By decreasing temperature below T(g) at ambient pressure or by elevating pressure above P(g), the glass transition pressure, at constant temperature, the excess wing of isoeugenol shifts to lower frequencies and is transformed into a secondary beta-loss peak, while in eugenol it becomes a shoulder. These spectral features enable the beta-relaxation time tau(beta) to be determined in the glassy state. These changes indicate that the excess wings in isoeugenol and eugenol are similar and both are secondary beta relaxations that are not resolved in the liquid state. While in both isoeugenol and eugenol the loss peak of the beta relaxation in the glassy state and the corresponding excess wing in the liquid state shifts to lower frequencies on elevating pressure, the locations of their gamma relaxation show little change with increasing pressure. The different pressure sensitivities of the excess wing and gamma relaxation are further demonstrated by the nearly perfect superposition of the alpha-loss peak together with excess wing from the data taken at ambient pressure and at elevated pressure (and higher temperature so as to have the same alpha-peak frequency), but not the gamma-loss peak in both isoeugenol and eugenol. On physical aging isoeugenol, the beta-loss peak shifts to lower frequencies, but not the gamma relaxation. Basing on these experimental facts, the faster gamma relaxation is a local intramolecular process involving a side group and the slower beta relaxation mimics the structural alpha relaxation in behavior, involves the entire molecule and satisfies the criteria for being the Johari-Goldstein beta relaxation. Analysis and interpretation of the spectra utilizing the coupling model further demonstrate that the excess wings seen in the equilibrium liquid states of these two isomers are their genuine Johari-Goldstein beta relaxation.

The myogenic response is suppressed in cerebral arteries of caveolin‐1 deficient mice

Caveolins are caveolae localized proteins that regulate cardiovascular physiology and pathology. Here, we explored the function of caveolin-1 (cav-1) in the myogenic response using cerebral arteries of cav-1 deficient (cav-1−/ −) mice. At an intravascular pressure of 10 mmHg, myogenic tone was similar in wild-type (cav-1+/+) and cav-1−/ −arteries (% tone: cav-1+/+: 2.8±0.6 vs. cav-1−/ −: 1.4±0.3). However, at pressures between 30 and 70 mmHg, cav-1−/ −arteries developed less myogenic tone (% tone at 70 mmHg: cav-1+/+: 19.3±0.5 vs. cav-1−/ −: 12.0±0.7). At 10 mmHg, membrane potential was similar in cav-1+/+ (−59±3 mV) and cav-1−/ − (−62±3 mV) arteries. In contrast, a pressure elevation to 50 mmHg depolarized cav-1+/+ arteries to −33±1 mV, whereas cav-1−/ − arteries only depolarized to −43±2 mV. At 10 mmHg, arterial wall intracellular Ca2+ ([Ca2+]i) concentration was also similar in cav-1+/+ (73±15 nM) and cav-1−/ − (80±18 nM) arteries. However, elevating pressure to 70 mmHg increased arterial wall [Ca2+]i concentration to 320±29 nM in cav-1+/+, but to only 206±25 nM in cav-1−/ − arteries. Extracellular Ca2+removal and diltiazem (50 μM), an L-type Ca2+channel blocker, similarly reduced [Ca2+]i and dilated pressurized cav-1+/+ and cav-1−/ −arteries. L-NNA, a nitric oxide synthase inhibitor, partially, but did not fully restore the tone difference between cav-1+/+ and cav-1−/ − arteries. In summary, data indicate that cav-1 ablation attenuates pressure-induced membrane depolarization, which reduces the arterial wall [Ca2+]i elevation and constriction in cerebral arteries.

고압 및 고진공에서의 피리딘과 벤조일클로라이드류의 반응에 관한 속도론적 연구

아세토니트릴 용매내에서 파라치환 염화벤조일류(<TEX>$p-CH_3$</TEX>, p-H, <TEX>$p-NO_2$</TEX>)와 피리딘의 반응속도를 온도와 압력변화에 따라 전기전도도법으로 측정하여 유사 1차반응속도상수와 2차반응속도상수를 구하였다. 이들 반응속도상수로부터 활성화파라미터들(<TEX>${\Delta}V{\ddagger},\;{\Delta}{\beta}{\ddagger},\;{\Delta}H{\ddagger},\;{\Delta}S{\ddagger},\;{\Delta}G{\ddagger}$</TEX> 과 Hammett <TEX>${\rho}$</TEX>를 구하였다. 이때 <TEX>${\Delta}V{\ddagger},\;{\Delta}{\beta}{\ddagger}$</TEX> 및 <TEX>${\Delta}S{\ddagger}$</TEX>는 모두 음의 값을 나타내었으며, 모든 압력 조건에서 기질의 치환기효과 <TEX>${\rho}_Y$</TEX>는 양의 값을 나타내었다. 압력과 치환기 변화에 따른 속도론적 연구를 종합하면, 전체적인 반응은 전형적인 <TEX>$SN_2$</TEX> 반응메카니즘을 따르며, 압력 증가에 따라 결합 형성이 더욱 촉진된 반응메카니즘으로 진행됨을 알 수 있다. The reaction rates of para-substituted benzoyl chlorides (<TEX>$p-CH_3$</TEX>, p-H, <TEX>$p-NO_2$</TEX>) with pyridine have been measured employing the conductometry method in acetonitrile. The pseudo first-order and second-order rate constants were determined at various pressures and temperatures. The activation parameters (<TEX>${\Delta}V{\ddagger},\;{\Delta}{\beta}{\ddagger},\;{\Delta}H{\ddagger},\;{\Delta}S{\ddagger},\;{\Delta}G{\ddagger}$</TEX>) and the Hammett <TEX>${\rho}$</TEX>-values are determined from the values of rate constant. The values of <TEX>${\Delta}V{\ddagger},\;{\Delta}{\beta}{\ddagger}\;and\;{\Delta}S{\ddagger}$</TEX> are all negative. The Hammett <TEX>${\rho}$</TEX>-values are positive for the substrate (<TEX>${\rho}_Y$</TEX>) over the given pressure range. The results of kinetic studies, for the pressure and substituent changes, show that these reactions are proceeded by a typical <TEX>$SN_2$</TEX>reaction mechanism and its bond formation is favored with elevating pressure.

Changes in rabbit skeletal myosin and its subfragments under high hydrostatic pressure

The pressure-induced denaturation of rabbit skeletal myosin and its subfragments under hydrostatic pressure were investigated. Four nanometer of red shift of the intrinsic fluorescence spectrum was observed in myosin under a pressure of 400 MPa. The ANS fluorescence of myosin increased with elevating pressure. Changes in the intrinsic fluorescence spectra of myosin and its subfragments were quantified and expressed as the center of spectral mass. The center of spectral mass of myosin and its subfragments linearly decreased with elevating pressure, and increased with lowering pressure. The fluorescence intensity of the ANS-labeled rod did not change during pressure treatment. The present results indicate that the most pressure-sensitive portion of myosin molecule is the head. Hysteresis of the center of spectral mass of S1 appeared under pressures above 300 MPa. Changes in the center of spectral mass of S1 above 350 MPa showed stronger hysteresis. The center of spectral mass did not decrease above 350 MPa during the compression process, indicating that S1 was stable in a partially denatured state at 350 MPa under pressure. The changes in the relative intensities of ANS fluorescence of S1 were measured under pressures up to 400 MPa, and the ANS fluorescence intensity increased with elevating pressure but it did not change after pressure release. The ANS fluorescence intensity increased under constant pressure suggesting that the pressure-induced denaturation of myosin was accelerated during pressurization.

Effect of high hydrostatic pressure on chicken myosin subfragment-1

Hydrostatic pressure-induced structural changes in subfragment-1 (S1) of myosin molecule were studied. ATP-induced emission spectra of S1 were used to detect global structural change of S1 by pressure treatment. The fluorescence intensity of unpressurized S1 increased by addition of ATP. The increment of fluorescence of pressurized S1 up to 150 MPa was almost the same as control, whereas it became smaller above 200 MPa. ATP binding ability of S1 examined using 1, N 6-ethenoadenosine 5′-diphosphate (ε-ADP) indicated that the binding of ε-ADP to S1 decreased in the range of 250–300 MPa. S1 pressurized below 250 MPa and unpressurized S1 similarly bound to F-actin, although binding of S1 pressurized above 250 MPa decreased. Electron microscopic observation revealed arrowhead structure in control acto-S1, while disordered arrowhead structure was observed in acto-S1 prepared from pressurized S1 at 300 MPa. S1 pressurized below 250 MPa retained the same actin activated ATPase activity as the control, whereas the activity decreased to 60% at 300 MPa. Pressure treated S1 was easily cleaved by tryptic digestion into three domains, i.e. 27 kDa (N-terminal), 50 and 20 kDa (C-terminal) fragments, which were the same as those in unpressurized one. It is concluded that pressure-induced global structural changes of S1 begin to occur about 150 MPa, and the local structural changes in ATPase and actin binding sites followed with elevating pressure to 250–300 MPa.

Effect of pressure gradient on heat transfer of impinging submerged circular jets

An experimental and numerical study have been carried out to investigate the distribution of radial local heat transfer coefficients of impinging submerged circular jets. Good agreement is achieved between the experimental results and the predicted value. Results show that the outer peak usually occurs at the radial location of r/d=1.8–2.0, in which transition from laminar to turbulence happens resulting from disappeared pressure gradient abruptly, and that the inner peak appears rigidly at r/d=0.5, where the boundary layer has a minimum thickness because of elevating pressure gradient.

Necrotizing Fasciitis: An Overview

For numerous reasons, the number of cases of necrotizing fasciitis is increasing. Several bacteria can be responsible for the destruction of subcutaneous tissue and fat, including group A streptococcus. Immunosuppressed individuals, diabetics, males, and the aged comprise the largest susceptible groups. Further muscle and nerve necrosis occurs secondary to compartment syndrome and elevating pressure. After surgical debridement, appropriate antibiotic therapy, and healing of necessary skin grafts, residual loss of function may require the use of an orthosis. The practicing orthotist needs to understand the cause, course, and functional limitations of necrotizing fasciitis in order to produce a successful orthotic outcome.

Effects of hydrostatic pressure on the structure and biological activity of infectious bursal disease virus.

The effects of high hydrostatic pressure on the structure and biological activity of infectious bursal disease virus (IBDV), a commercially important pathogen of chickens, were investigated. IBDV was completely dissociated into subunits at a pressure of 240 MPa and 0 degrees C revealed by the change in intrinsic fluorescence spectrum and light scattering. The dissociation of IBDV showed abnormal concentration dependence as observed for some other viruses. Electron microscopy study showed that morphology of IBDV had an obvious change after pressure treatment at 0 degrees C. It was found that elevating pressure destroyed the infectivity of IBDV, and a completely pressure-inactivated IBDV could be obtained under proper conditions. The pressure-inactivated IBDV retained the original immunogenic properties and could elicit high titers of virus neutralizing antibodies. These results indicate that hydrostatic pressure provides a potential physical means to prepare antiviral vaccine.

Bubble flow characteristics in bubble columns at elevated pressure and temperature

AbstractHydrodynamic characteristics of bubble columns are studied by considering both the local/bubble‐scale and global/column‐scale properties of the system, with specific emphasis on their dependency on operating pressure and temperature. The local‐scale properties include single‐bubble characteristics and interactive dynamics involving bubble coalescence and breakup, while the global‐scale properties include gas holdup. Experiments are conducted in a bubble column with a multiorifice ring sparger for pressures as high as 20 MPa and temperatures ranging from 27 to 78°C. Density, viscosity, and surface tension, the liquid phase properties, are measured in situ by using hydrostatic weighing, falling‐ball and emerging‐bubble techniques, respectively. The bubble behavior is examined through direct‐flow visualization. Pressure and temperature affect the bubble rise velocity mainly by varying physical properties of the fluids. Effects of pressure and temperature on the rates of bubble formation, coalescence and breakup, and the initial bubble size and maximum stable bubble size are illustrated. Elevating pressure and/or temperature increases gas holdup; the increasing rate depends on the operating conditions through their effects on the fluid physical properties.

The Effects of Exercise Training on Salt-Induced Hypertension in the Borderline Hypertensive Rat

The borderline hypertensive rat (BHR) develops severe hypertension when chronically subjected to either a high salt diet or behavioral stress. Previous research has shown that daily exercise can attenuate the development of stress-induced hypertension in the BHR. The current study sought to determine whether exercise might also exert a similar protective effect on salt-induced hypertension. Two groups of BHR were placed on a high salt diet for 20 weeks; one of the groups also engaged in daily swim training for the entire 20 week period. A third group of BHR served as maturation controls. At the end of the experimental period, direct measurement of heart rate in conscious subjects revealed a significant resting bradycardia in the trained group on a high salt diet but no significant group differences with respect to blood pressure level. Cardiovascular responses to an episode of acute stress revealed that BHR are capable of elevating pressure in response to a novel stressor after swim training. These observations suggest that exercise may be an environmental intervention capable of increasing cardiovascular responses to acute stressors.

Further studies on the effect of ephedrine on the circulation: Chen, K. K., and Meek, Walter J.: Jour. Pharmacol. and Exper. Therap., 1926, xxviii, 31

1. Ephedrine given intravenously in anesthetized dogs in the dosage from 0.005 to 30 mgm. per kilo, raises arterial blood pressure, the optimum dose lying between 1 and 10 mgm. per kilo. Larger doses usually lower the blood pressure. The change in pressure does not entirely depend on the quantity given, but also on the condition of the animal prior to its administration. Repeated intravenous injections of optimum doses, when given at intervals of twenty-five minutes, are not as effective as the first in raising blood pressure in regard to duration and height. Repeated intravenous injections of sub-optimum doses, on the other hand, when given close together will show a summative effect in elevating pressure. 2. Ephedrine in stimulating doses (those that raise blood pressure) given intravenously; intramuscularly, orally or subcutaneously, in anesthetized or non-anesthetized animals with intact vagi usually slows the pulse rate. Acceleration always takes place when the vagi are paralyzed by atropine. Ephedrine in depressing doses (those that lower the blood pressure) always decreases the pulse rate irrespective of the condition of the vagi. 3. Prolonged vasoconstriction is observed in the perfusion of isolated mammalian organs. In plethysmographic studies, it is found that the splenic vessels are constricted, the renal vessels first constricted then dilated, and the intestinal and leg vessels usually dilated. The rise of blood pressure cannot therefore be entirely due to peripheral constriction. Cardiac stimulation, as concluded before, is one of the factors. 4. Ephedrine sulphate applied locally to the frog's heart may accelerate the heart rate by a few beats per minute in a concentration of 1:1000, but depresses it both in rate and amplitude in a concentration of 1:100. In the perfusion of the terrapin's heart, ephedrine sulphate may accelerate the rate by a few beats per minute in a concentration of 1:10,000, but produces bradycardia and usually a decrease in amplitude in concentrations of 1:1000 and 1:100, with frequent occurrence of auricular extrasystoles, and finally passing to a state of feeble contractions followed by standstill at diastole. Perfusion experiments of the isolated rabbit's heart by Langendorff's method shows that ephedrine sulphate dissolved in Locke's solution stimulates the heart by increasing both the rate and the strength of contractions in a concentration of 1:100,000, but depresses both in concentrations of 1:10,000 and 1:5000. Concentrations of 1:2000 and 1:1000 bring about partial block, the latter finally causing stoppage. Colloidal solutions, such as peptone or horse serum added to Locke's solution, reduce the depressant action of ephedrine. 5. By electrocardiographic studies in non-anesthetized and anesthetized dogs, small doses of ephedrine given intravenously cause nothing more than some alteration of the T wave—flattening, reversion or occasionally augmentation. Massive doses in dogs and rabbits appear to depress the automatic and conductive system in a descending order; that is, from the S-A node to the terminations of the Purkinje system. There is, therefore, an occurrence of bradycardia, prolongation of the P-R interval, partial A-V block, nodal rhythm, ventricular escape or extrasystoles, bundle branch block and finally ventricular fibrillation. 6. With the vagal reflex abolished in anesthetized dogs, ephedrine is shown to increase the cardiac output during the rise of blood pressure and increase of pulse rate. It decreases slightly the diastolic size of the heart, as measured from x-ray plates, which, however, does not seem to be sufficient to overbalance the increase of volume output since a very marked increase of pulse rate is produced.