Four-point probe measurements using current probes with voltage feedback to measure electric potentials

We present a four-point probe resistance measurement technique which uses four equivalent current measuring units, resulting in minimal hardware requirements and corresponding sources of noise. Local sample potentials are measured by a software feedback loop which adjusts the corresponding tip voltage such that no current flows to the sample. The resulting tip voltage is then equivalent to the sample potential at the tip position. We implement this measurement method into a multi-tip scanning tunneling microscope setup such that potentials can also be measured in tunneling contact, allowing in principle truly non-invasive four-probe measurements. The resulting measurement capabilities are demonstrated for BiSbTe$_3$ and Si$(111)-(7\times7)$ samples

Thermoplastic deformation of silicon surfaces induced by ultrashort pulsed lasers in submelting conditions

A hybrid 2D theoretical model is presented to describe thermoplastic deformation effects on silicon surfaces induced by single and multiple ultrashort pulsed laser irradiation in submelting conditions. An approximation of the Boltzmann transport equation is adopted to describe the laser irradiation process. The evolution of the induced deformation field is described initially by adopting the differential equations of dynamic thermoelasticity while the onset of plastic yielding is described by the von Mise's stress. Details of the resulting picometre sized crater, produced by irradiation with a single pulse, are then discussed as a function of the imposed conditions and thresholds for the onset of plasticity are computed. Irradiation with multiple pulses leads to ripple formation of nanometre size that originates from the interference of the incident and a surface scattered wave. It is suggested that ultrafast laser induced surface modification in semiconductors is feasible in submelting conditions, and it may act as a precursor of the incubation effects observed at multiple pulse irradiation of materials surfaces.Comment: To appear in the Journal of Applied Physic

What role does phosphorylation of cardiac troponin I play in elevating cardiac contractility following adrenergic stimulation?

Abstract only availableMyocardial performance is enhanced when adrenergic receptors are stimulated by catecholamines. The enhanced performance is mediated by cAMP dependent protein kinase A (PKA), which phosphorylates several proteins within the cardiac myocyte including cardiac troponin I (cTnI) and myosin binding protein-C (MyBP-C). Phosphorylation of these two proteins by PKA appears to mediate inotropic effects of adrenergic stimulation by directly modulating the rate of cross-bridge cycling. For instance, phosphorylation of cTnI and MyBP-C by PKA increased the power generating capacity of single permeabilized cardiac myocyte preparations (Herron, Korte, McDonald Circ Res 89;1184-1190:2001). It is unknown whether phosphorylation of cTnI or MyBP-C alone or phosphorylation of both proteins is necessary to increase power. The purpose of this study was to develop a methodology to test the relative importance of the two PKA phosphorylation sites on cTnI (serine 23 and 24) in mediating the PKA induced increase in myocyte power output. For these experiments, serines 23 and 24 of rat cTnI cDNA were mutated to alanines using site directed mutagenesis. Next, mutated cTnI (cTnI23/24) was expressed in E. coli bacteria and purified using ion exchange chromatography. Mutated cTnI (cTnI23/24) was then complexed with purified cTnT and cTnI and this whole troponin (cTn) complex was exchanged for endogenous cTn in permeabilized cardiac myocytes overnight using a cTn exchange buffer (20 mM Imidazole, 200 mM KCl, 5 mM EGTA, 5 mM MgCl2, 1 mM DTT). The extent of cTn exchange was assessed by quantifying the amount of PKA-induced phosphate incorporation. We observed only a partial reduction in PKA-induced phosphate incorporation following exhange of cTnI23/24, implicating only a partial Tn exchange using these conditions. We are currently seeking to increase the extent of cTnI23/24 exchange after which individual myocyte preparations will be mounted between a force transducer and position motor and myocyte power output generating capacity will be measured before and after PKA induced phosphorylation of myofilament proteins. These experiments will directly assess whether phosphorylation of cTnI by PKA is necessary to elevate myocyte power output.Life Sciences Undergraduate Research Opportunity Progra

Estimation of the threat of IEMI to complex electronic systems

The threat of ultra wideband (UWB) sources is interesting for military issues. This paper summarizes information concerning the voltages generated from some commercially available UWB generator systems and their produced electromagnetic fields. The paper focuses on the coupling of UWB fields into electronic equipment and discusses possible modeling and measurement techniques to estimate such a threat for modern ships. An evaluation procedure for the determination of the induced voltage at the input of an electronic component is presented. This method is based on the computation of the internal electric field and the measurements on a test network, which is similar to the structure of the steering control cabling. It allows the estimation of the potential threat for the ship's electronic equipment due to the exposal to UWB emitting sources

Shielding of electronic systems against transient electromagnetic interferences

In order to protect electronic systems against the effects of transient electromagnetic interferences, shields made of electrically conductive material can be used. The subject of this paper is an electrically conductive textile. When applying the shield, a reliable measure is needed in order to determine the effectiveness of the shield to protect against electromagnetic pulses. For this purpose, a time domain measurement technique is presented using double exponential pulses. With these pulses, the susceptibility of an operating electronic device with and without the shield is determined. As a criterion of quality of a shield, the breakdown failure rate found in both cases is compared. © 2004 Copernicus GmbH

Power Output Is Increased After Phosphorylation of Myofibrillar Proteins in Rat Skinned Cardiac Myocytes

This work was supported by American Heart Association Beginning Grant-in-Aid 9914291 and NIH Grant HL57852.The publisher's version may be found at http://circres.ahajournals.org/cgi/content/full/89/12/1184ß-Adrenergic stimulation increases stroke volume in mammalian hearts as a result of protein kinase A (PKA)-induced phosphorylation of several myocyte proteins. This study investigated whether PKA-induced phosphorylation of myofibrillar proteins directly affects myocyte contractility. To test this possibility, we compared isometric force, loaded shortening velocity, and power output in skinned rat cardiac myocytes before and after treatment with the catalytic subunit of PKA. Consistent with previous studies, PKA increased phosphorylation levels of myosin binding protein C and troponin I, and reduced Ca2+ sensitivity of force. PKA also significantly increased both maximal force (25.4±8.3 versus 31.6±11.3 µN [P<0.001, n=12]) and peak absolute power output (2.48±1.33 versus 3.38±1.52 µW/mg [P<0.05, n=5]) during maximal Ca2+ activations. Furthermore, PKA elevated power output at nearly all loads even after normalizing for the increase in force. After PKA treatment, peak normalized power output increased {approx}20% during maximal Ca2+ activations (n=5) and {approx}33% during half-maximal Ca2+ activations (n=9). These results indicate that PKA-induced phosphorylation of myofibrillar proteins increases the power output-generating capacity of skinned cardiac myocytes, in part, by speeding the step(s) in the crossbridge cycle that limit loaded shortening rates, and these changes likely contribute to greater contractility in hearts after ß-adrenergic stimulation

Mechanical properties and deformation mechanisms of manganese sulphide inclusions

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