Secret

For weeks we have been sitting here in this position. The camouflage nets have been draped over each vehicle, looking like a nightmare out of the Arabian Nights, for weeks now. Everything has a harried, slovenly look, but maybe it\u27s because this is a secret position. When we were ordered up here, it was under the heaviest cloak of secrecy. All identification was removed from the trucks, each man was inspected for any signs of which outfit he belonged to; they went through our clothing for addresses or cards. This was big, we had been told. We were to cross the Ruhr River and then it shouldn\u27t be too long before the Germans caught onto how useless it was to try to keep on fighting

Fuel Composition Analysis of Endothermically Heated JP-8 Fuel for Use in a Pulse Detonation Engine

Waste heat from a pulse detonation engine (PDE) was extracted via zeolite catalyst coated concentric tube-counter flow heat exchangers to produce supercritical pyrolytic conditions for JP-8 fuel. A sampling system and method were developed that enabled samples of reacted fuel to be extracted during steady state operation. Samples were taken over a range of heat exchanger exit temperatures from 820 K (1016° F) to 940 K (1232° F). Offline analysis of liquid and vapor fuel samples indicated fuel decomposition via typical pyrolytic reaction pathways. The liquid analysis showed conversion of parent fuel components with formation of unsaturates (aromatics and alkenes) and smaller alkanes. The gaseous products consisted of predominantly C1-C3 alkanes and alkenes (\u3e 75% of total vapor yield) with moderate amounts of hydrogen and C4-C6 alkanes and alkenes. The components that were present in the stressed fuel samples were more detonable and could be linked to improved PDE performance. The ignition time decreased by over 20% as temperature increased from 820 K (1016° F) to 935 K (1224° F) and by more than 30% when compared to unreacted (flash vaporized) JP-8

Kierkegaard's Irony in the "Diapsalmata"

Kierkegaard's Irony in the "Diapsalmata

The assembly of yeast mitochondrial ATP synthase: subunit depletion in vivo suggests ordered assembly of the stalk subunits b, OSCP and d

AbstractThe abundance in vivo of each of three subunits b, OSCP and d, components of the stalk region of the yeast mitochondrial ATP synthase complex, was manipulated by a controlled depletion strategy. Western blots of whole cell lysates were used to study the effect of depletion of each of these subunits on the cellular levels of other subunits of the enzyme complex. A hierarchy of subunit stability was determined and interpreted to indicate the order of assembly of these three subunits of the stalk region. Thus, subunit b is assembled first, followed by OSCP and then by subunit d

Lack of correlation between MYCN expression and the Warburg effect in neuroblastoma cell lines

<p>Abstract</p> <p>Background</p> <p>Many cancers preferentially meet their energy requirements through the glycolytic pathway rather than via the more efficient oxidative phosphorylation pathway. It is thought that this is an important adaptation in cancer malignancy. We investigated whether use of glycolysis for energy production even in the presence of oxygen (known as the Warburg effect) varied between neuroblastoma cell lines with or without <it>MYCN </it>amplification (a key indicator of poor disease outcome in neuroblastoma).</p> <p>Methods</p> <p>We examined ATP and lactate production, oxygen consumption and mitochondrial energisation status for three neuroblastoma cell lines with varying degrees of <it>MYCN </it>amplification and MYCN expression.</p> <p>Results</p> <p>We found no correlation between MYCN expression and the Warburg effect in the cell lines investigated.</p> <p>Conclusion</p> <p>Our results suggest preferential use of glycolysis for energy production and MYCN expression may be independent markers of neuroblastoma malignancy <it>in vitro </it>if not <it>in vivo</it>.</p

Coenzyme Q10 therapy before cardiac surgery improves mitochondrial function and in vitro contractility of myocardial tissue

AbstractObjectivesPrevious clinical trials suggest that coenzyme Q10 might afford myocardial protection during cardiac surgery. We sought to measure the effect of coenzyme Q10 therapy on coenzyme Q10 levels in serum, atrial trabeculae, and mitochondria; to assess the effect of coenzyme Q10 on mitochondrial function; to test the effect of coenzyme Q10 in protecting cardiac myocardium against a standard hypoxia-reoxygentation stress in vitro; and to determine whether coenzyme Q10 therapy improves recovery of the heart after cardiac surgery.MethodsPatients undergoing elective cardiac surgery were randomized to receive oral coenzyme Q10 (300 mg/d) or placebo for 2 weeks preoperatively. Pectinate trabeculae from right atrial appendages were excised, and mitochondria were isolated and studied. Trabeculae were subjected to 30 minutes of hypoxia, and contractile recovery was measured. Postoperative cardiac function and troponin I release were assessed.ResultsPatients receiving coenzyme Q10 (n = 62) had increased coenzyme Q10 levels in serum (P = .001), atrial trabeculae (P = .0001), and isolated mitochondria (P = .0002) compared with levels seen in patients receiving placebo (n = 59). Mitochondrial respiration (adenosine diphosphate/oxygen ratio) was more efficient (P = .012), and mitochondrial malondialdehyde content was lower (P = .002) with coenzyme Q10 than with placebo. After 30 minutes of hypoxia in vitro, pectinate trabeculae isolated from patients receiving coenzyme Q10 exhibited a greater recovery of developed force compared with those in patients receiving placebo (46.3% ± 4.3% vs 64.0% ± 2.9%, P = .001). There was no between-treatment difference in preoperative or postoperative hemodynamics or in release of troponin I.ConclusionsPreoperative oral coenzyme Q10 therapy in patients undergoing cardiac surgery increases myocardial and cardiac mitochondrial coenzyme Q10 levels, improves mitochondrial efficiency, and increases myocardial tolerance to in vitro hypoxia-reoxygenation stress

Bim Links ER Stress and Apoptosis in Cells Expressing Mutant SOD1 Associated with Amyotrophic Lateral Sclerosis

Endoplasmic reticulum (ER) stress is an important pathway to cell death in amyotrophic lateral sclerosis (ALS). We previously demonstrated that ER stress is linked to neurotoxicity associated with formation of inclusions of mutant Cu,Zn-superoxide dismutase 1 (SOD1). Cells bearing mutant inclusions undergo mitochondrial apoptotic signalling. Here, we demonstrate that the BH3-only protein, Bim, is a direct link between ER stress and mitochondrial apoptosis. In the murine neuroblastoma cell line, Neuro2a, bearing mutant SOD1 inclusions, indicators of both ER stress and apoptosis are expressed. Bim knockdown by siRNA significantly reduced nuclear apoptotic features in these inclusion-bearing cells (but did not affect the proportion of cells overall that bear inclusions). Further, both Bax recruitment to mitochondria and cytochrome c redistribution were also decreased under Bim-depletion conditions. However, upregulation of CHOP, a marker of ER stress, was not reduced by Bim knockdown. Significantly, knockdown of CHOP by siRNA reduced the extent of apoptosis in cells bearing mutant SOD1 inclusions. These sequential links between ER stress, CHOP upregulation, and Bim activation of mitochondrial apoptotic signalling indicate a clear pathway to cell death mediated by mutant SOD1