Assessing the Acceptability of Science Operations Concepts and the Level of Mission Enhancement of Capabilities for Human Mars Exploration Extravehicular Activity.

The Biologic Analog Science Associated with Lava Terrains (BASALT) research project is investigating tools, techniques, and strategies for conducting Mars scientific exploration extravehicular activity (EVA). This has been accomplished through three science-driven terrestrial field tests (BASALT-1, BASALT-2, and BASALT-3) during which the iterative development, testing, assessment, and refinement of concepts of operations (ConOps) and capabilities were conducted. ConOps are the instantiation of operational design elements that guide the organization and flow of personnel, communication, hardware, software, and data products to enable a mission concept. Capabilities include the hardware, software, data products, and protocols that comprise and enable the ConOps. This paper describes the simulation quality and acceptability of the Mars-forward ConOps evaluated during BASALT-2. It also presents the level of mission enhancement and acceptability of the associated Mars-forward capabilities. Together, these results inform science operations for human planetary exploration.

Halo structure of (14)Be.

The two-neutron halo nucleus (14)Be has been investigated in a kinematically complete measurement of the fragments ((12)Be and neutrons) produced in dissociation at 35 MeV/nucleon on C and Pb targets. Two-neutron removal cross sections, neutron angular distributions, and invariant mass spectra were measured, and the contributions from electromagnetic dissociation (EMD) were deduced. Comparison with three-body model calculations suggests that the halo wave function contains a large nu(2s(1/2))(2) admixture. The EMD invariant mass spectrum exhibited enhanced strength near threshold consistent with a nonresonant soft-dipole excitation.

Effect of lipid feeding on endothelium dependent relaxation in rabbit aortic preparations.

The effect of a cholesterol enriched diet on concentration responses to 5-hydroxytryptamine, ergometrine, and acetylcholine and on endothelium dependent relaxation was investigated in rabbit aortic strip preparations. Sensitivity to ergometrine was slightly reduced after both two and 10 weeks of cholesterol feeding. Sensitivity to 5-hydroxytryptamine was slightly reduced after two but not after 10 weeks of cholesterol feeding. Sensitivity to acetylcholine was not altered at two or 10 weeks in the absence of endothelium, but the endothelium dependent lowering of the constrictor concentration-response was almost abolished after 10 weeks of cholesterol feeding. Likewise the endothelium dependent relaxant response of preconstricted preparations to acetylcholine was almost abolished after 10 weeks of cholesterol feeding. Thus this model of hyperlipidaemia leads after 10 weeks to loss of endothelium dependent relaxation.

Differences in basal endothelium-derived relaxing factor activity in different artery types.

Mechanical responses and calcium influx were measured in order to compare basal endothelium-derived relaxing factor (EDRF) activity in isolated preparations of rabbit aorta, rat aorta, and dog coronary artery. EDRF activity was characterized by endothelium-dependent mechanical relaxation and reduction of 45Ca influx which could be blocked by EDRF inhibitors. In resting preparations, the mechanical effects of basal EDRF were negligible in all preparations, and a small effect on calcium influx was demonstrated only in rat preparations. In agonist-constricted preparations, basal EDRF activity had only a small mechanical effect in rabbit preparations but markedly depressed constriction in rat and dog preparations; likewise, it had no demonstrable effect on calcium influx in rabbit preparations but had a marked effect in rat and dog preparations. In both resting and agonist-stimulated rabbit preparations, endothelium caused a cyclooxygenase product-dependent increase in calcium influx. Thus, basal EDRF activity has little or no effect in resting preparations and little or no effect in agonist-stimulated rabbit aorta preparations, but a marked effect in agonist-stimulated rat aorta and dog coronary preparations.

Myocardial reoxygenation damage: can it be circumvented?

We investigated whether reoxygenation damage could be prevented by interventions directed towards reducing calcium influx only during the reoxygenation period. We measured reoxygenation contracture and recovery of contractile performance, using isolated papillary muscle preparations from cat and rabbit, pretreated with ouabain so as to exaggerate the phenomenon of reoxygenation contracture. Reoxygenation contracture was abolished and contractile recovery achieved by lowering extracellular calcium during early reoxygenation and then gradually replacing it. Gradual reoxygenation only postponed contracture and contractile failure. The slow channel blocker, diltiazem, but not verapamil or lidoflazine--in similarly negative inotropic concentrations of 10(-4) mol X litre-1, 10(-4) mol X litre-1 and 2 X 10(-5) mol X litre-1 respectively--reduced early reoxygenation contracture, as did Mg2+ (30 mmol X litre-1), Mn2+ (8 mmol X litre-1), or metabolic acidosis (pH 6.5), without in any case allowing contractile recovery. These observations indicate that reoxygenation damage is not an irrevocable consequence of the preceding hypoxic insult. They imply that calcium entry during early reoxygenation contributes both to contracture and contractile failure, that this occurs through paths other than the slow calcium channel, and that diltiazem may have properties additional to those of blocking the slow calcium channel.

Frequency-dependent depression of myocardial contractility by slow calcium channel blocking drugs.

The negative inotropic effects of two dihydropyridine and two non-dihydropyridine calcium slow channel blocking drugs were studied using ferret isolated papillary muscle preparations contracting both isotonically and isometrically. The degree of inotropic depression was found to be dependent on the frequency of stimulation for all four agents. Frequency dependence of inotropic effect was of the order: nifedipine less than felodipine less than diltiazem less than verapamil.

Myocardial reoxygenation damage. Can it be circumvented?

Isolated papillary-muscle preparations from the cat and rabbit were used to study the phenomenon of reoxygenation contracture and whether is is amenable to intervention independently of the preceding hypoxic insult. Reduction of extracellular Ca2+ to "0" mM abolished reoxygenation contracture, but subsequent replacement of Ca2+ resulted in severe contracture and death due to the "calcium paradox." Lowering of Ca2+ to 0.125 mM and its stepwise replacement to 2.5 mM resulted in no contracture with good mechanical recovery. Gradual reoxygenation, Mg2+ (30 mM), Mn2+ (8 mM), or H+ (pH 6.5) ions, or diltiazem (10(-4) M) delayed but did not prevent the development of contracture and contractile failure. Unlike diltiazem, verapamil (10(-4) M) and lidoflazine (2 X 10(-5) M) did not significantly affect the contracture.