307 research outputs found

    Combined Effect of Contraction Ratio and Chamber Pressure on the Performance of a Gaseous Hydrogen-Liquid-Oxygen Combustor for a Given Propellant Weight Flow and Oxidant-Fuel Ratio

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    The effect of contraction ratio and chamber pressure on the combustion performance of a gaseous-hydrogen-liquid-oxygen combustor was investigated analytically and experimentally. The experiment was conducted with a "two-dimensional" gaseous-hydrogen-liquid-oxygen engine of about 150-pound thrust. The contraction ratio was varied from 1.5 to 6 by changing the nozzle throat area. This variation resulted in a chamber pressure variation of about 25 to 120 pounds per square inch. The experimental results were corrected for heat transfer to the engine walls and momentum pressure losses. The experimental performance, as evaluated in terms of characteristic exhaust velocity, was 98 percent of theoretical at contraction ratios greater than 3 but decreased very rapidly at smaller contraction ratios. The heat-transfer rate increased with increasing contraction ratio and chamber pressure; it was about 1 Btu per square inch per second at a contraction ratio of 1.5 and increased to about 3 at a contraction ratio of 6. The combined effects of contraction-ratio and chamber-pressure changes on performance were investigated analytically with a mixing model and a vaporization model. The mixing model predicted very poor mixing at contraction ratios below 3 and almost perfect mixing at higher contraction ratios. The performance predicted by the vaporization model was very close to 100 percent for all contraction ratios. From these results, it was concluded that the performance was limited by poor mixing at low contraction ratios and chamber pressures

    Propellant Vaporization as a Criterion for Rocket-Engine Design; Experimental Performance, Vaporization and Heat-Transfer Rates with Various Propellant Combinations

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    Experimental combustion efficiencies of eleven propellant combinations were determined as a function of chamber length. Efficiencies were measured in terms of characteristic exhaust velocities at three chamber lengths and in terms of gas velocities. The data were obtained in a nominal 200-pound-thrust rocket engine. Injector and engine configurations were kept essentially the same to allow comparison of the performance. The data, except for those on hydrazine and ammonia-fluorine, agreed with predicted results based on the assumption that vaporization of the propellants determines the rate of combustion. Decomposition in the liquid phase may be.responsible for the anomalous behavior of hydrazine. Over-all heat-transfer rates were also measured for each combination. These rates were close to the values predicted by standard heat-transfer calculations except for the combinations using ammonia

    Pom1 gradient buffering through intermolecular auto-phosphorylation.

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    Concentration gradients provide spatial information for tissue patterning and cell organization, and their robustness under natural fluctuations is an evolutionary advantage. In rod-shaped Schizosaccharomyces pombe cells, the DYRK-family kinase Pom1 gradients control cell division timing and placement. Upon dephosphorylation by a Tea4-phosphatase complex, Pom1 associates with the plasma membrane at cell poles, where it diffuses and detaches upon auto-phosphorylation. Here, we demonstrate that Pom1 auto-phosphorylates intermolecularly, both in vitro and in vivo, which confers robustness to the gradient. Quantitative imaging reveals this robustness through two system's properties: The Pom1 gradient amplitude is inversely correlated with its decay length and is buffered against fluctuations in Tea4 levels. A theoretical model of Pom1 gradient formation through intermolecular auto-phosphorylation predicts both properties qualitatively and quantitatively. This provides a telling example where gradient robustness through super-linear decay, a principle hypothesized a decade ago, is achieved through autocatalysis. Concentration-dependent autocatalysis may be a widely used simple feedback to buffer biological activities

    Distinct levels in Pom1 gradients limit Cdr2 activity and localization to time and position division.

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    Where and when cells divide are fundamental questions. In rod-shaped fission yeast cells, the DYRK-family kinase Pom1 is organized in concentration gradients from cell poles and controls cell division timing and positioning. Pom1 gradients restrict to mid-cell the SAD-like kinase Cdr2, which recruits Mid1/Anillin for medial division. Pom1 also delays mitotic commitment through Cdr2, which inhibits Wee1. Here, we describe quantitatively the distributions of cortical Pom1 and Cdr2. These reveal low profile overlap contrasting with previous whole-cell measurements and Cdr2 levels increase with cell elongation, raising the possibility that Pom1 regulates mitotic commitment by controlling Cdr2 medial levels. However, we show that distinct thresholds of Pom1 activity define the timing and positioning of division. Three conditions-a separation-of-function Pom1 allele, partial downregulation of Pom1 activity, and haploinsufficiency in diploid cells-yield cells that divide early, similar to pom1 deletion, but medially, like wild-type cells. In these cells, Cdr2 is localized correctly at mid-cell. Further, Cdr2 overexpression promotes precocious mitosis only in absence of Pom1. Thus, Pom1 inhibits Cdr2 for mitotic commitment independently of regulating its localization or cortical levels. Indeed, we show Pom1 restricts Cdr2 activity through phosphorylation of a C-terminal self-inhibitory tail. In summary, our results demonstrate that distinct levels in Pom1 gradients delineate a medial Cdr2 domain, for cell division placement, and control its activity, for mitotic commitment

    Crystal structures of asymmetric ClpX hexamers reveal nucleotide-dependent motions in a AAA+ protein-unfolding machine

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    ClpX is a AAA+ machine that uses the energy of ATP binding and hydrolysis to unfold native proteins and translocate unfolded polypeptides into the ClpP peptidase. The crystal structures presented here reveal striking asymmetry in ring hexamers of nucleotide-free and nucleotide-bound ClpX. Asymmetry arises from large changes in rotation between the large and small AAA+ domains of individual subunits. These differences prevent nucleotide binding to two subunits, generate a staggered arrangement of ClpX subunits and pore loops around the hexameric ring, and provide a mechanism for coupling conformational changes caused by ATP binding or hydrolysis in one subunit to flexing motions of the entire ring. Our structures explain numerous solution studies of ClpX function, predict mechanisms for pore elasticity during translocation of irregular polypeptides, and suggest how repetitive conformational changes might be coupled to mechanical work during the ATPase cycle of ClpX and related molecular machines.National Institutes of Health (U.S.) (Grant number AI-15706

    Modular Equations and Distortion Functions

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    Modular equations occur in number theory, but it is less known that such equations also occur in the study of deformation properties of quasiconformal mappings. The authors study two important plane quasiconformal distortion functions, obtaining monotonicity and convexity properties, and finding sharp bounds for them. Applications are provided that relate to the quasiconformal Schwarz Lemma and to Schottky's Theorem. These results also yield new bounds for singular values of complete elliptic integrals.Comment: 23 page

    Control of substrate gating and translocation into ClpP by channel residues and ClpX binding

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    ClpP is a self-compartmentalized protease, which has very limited degradation activity unless it associates with ClpX to form ClpXP or with ClpA to form ClpAP. Here, we show that ClpX binding stimulates ClpP cleavage of peptides larger than a few amino acids and enhances ClpP active-site modification. Stimulation requires ATP binding but not hydrolysis by ClpX. The magnitude of this enhancement correlates with increasing molecular weight of the molecule entering ClpP. Amino-acid substitutions in the channel loop or helix A of ClpP enhance entry of larger substrates into the free enzyme, eliminate ClpX binding in some cases, and are not further stimulated by ClpX binding in other instances. These results support a model in which the channel residues of free ClpP exclude efficient entry of all but the smallest peptides into the degradation chamber, with ClpX binding serving to relieve these inhibitory interactions. Specific ClpP channel variants also prevent ClpXP translocation of certain amino-acid sequences, suggesting that the wild-type channel plays an important role in facilitating broad translocation specificity. In combination with previous studies, our results indicate that collaboration between ClpP and its partner ATPases opens a gate that functions to exclude larger substrates from isolated ClpP.National Institutes of Health (U.S.) (Grant number AI-15706

    Long-term striatal overexpression of GDNF selectively downregulates tyrosine hydroxylase in the intact nigrostriatal dopamine system.

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    Sustained neurotrophic factor treatment in neurodegenerative disorders such as Parkinson's disease is likely to affect both degenerating and intact neurons. To investigate the effect of long-term glial cell line-derived neurotrophic factor (GDNF) overexpression on intact nigrostriatal dopamine neurons, we injected a recombinant lentiviral vector encoding GDNF, or green fluorescent protein, in the right striatum of young adult rats. Thirteen months after viral injection GDNF levels were 4.5 ng/mg tissue in the striatum and 0.9 ng/mg in the substantia nigra as measured by ELISA, representing a 25-100-fold increase above control vector- or nontransduced tissue. GDNF overexpression significantly reduced tyrosine hydroxylase mRNA levels (by 39-72%) in the substantia nigra and ventral tegmental area neurons, and the optical density of tyrosine hydroxylase-immunoreactive innervation in the striatum was reduced by 25-52% with the most prominent reductions appearing caudally. No significant reduction was seen in striatal vesicular monoamine transporter 2-immunoreactivity or [3H]mazindole binding autoradiography to dopamine uptake sites, two other presynaptic markers in dopamine axon terminals. The striatal D1 and D2 receptor binding as determined by [3H]SCH23390 and [3H]spiperone binding, respectively, was unaltered relative to the intact side in both treatment groups. Preproenkephalin mRNA levels in postsynaptic striatal neurons, which increase upon removal of striatal dopamine, were also unaffected by the GDNF treatment. Taken together our findings indicate that sustained GDNF administration to intact nigrostriatal dopamine neurons selectively reduces tyrosine hydroxylase expression, without altering striatal dopamine transmission to the extent that compensatory changes in several other components related to dopamine storage and signalling occur
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