Electronic cooling of a submicron-sized metallic beam

We demonstrate electronic cooling of a suspended AuPd island using superconductor-insulator-normal metal tunnel junctions. This was achieved by developing a simple fabrication method for reliably releasing narrow submicron sized metal beams. The process is based on reactive ion etching and uses a conducting substrate to avoid charge-up damage and is compatible with e.g. conventional e-beam lithography, shadow-angle metal deposition and oxide tunnel junctions. The devices function well and exhibit clear cooling; up to factor of two at sub-kelvin temperatures.Comment: 4 pages, 3 figure

Load sensitive stable current source for complex precision pulsed electroplating

Electrodeposition is a highly versatile and well explored technology. However, it also depends strongly on the experience level of the operator. This experience includes the pretreatment of the sample, and the composition of the electrolyte settings of the plating parameters. Accurate control over the electroplating current is needed especially for the formation of small structures, where pulsed electrodeposition has proven to reduce many unwanted effects. To bring precision into the formation of optimal recipes, a highly flexible current source based on a microcontroller was developed. It allows a large variety of pulse waveforms, as well as maintaining a feedback loop that controls the current and monitors the output voltage, allowing for both galvanostatic (current driven) and potentiostatic (voltage driven) electrodeposition. The system has been implemented with multiple channels, permitting the simultaneous electrodeposition of multiple substrates in parallel. Being based on a microcomputer, the system can be programmed using predefined recipes individually for each channel, or even adapt the recipes during plating. All measurement values are continuously recorded for the purpose of documentation and diagnosis. The current source is based on a high power operational amplifier in a modified Howland current source configuration. This paper describes the functionality of the electrodeposition system, with a focus on the stability of the source current under different electrodeposition current densities and frequencies. The performance and high capability of the system is demonstrated by performing and analyzing two nontrivial plating applications

Childhood exposure due to the Chernobyl accident and thyroid cancer risk in contaminated areas of Belarus and Russia

The thyroid dose due to 131I releases during the Chernobyl accident was reconstructed for children and adolescents in two cities and 2122 settlements in Belarus, and in one city and 607 settlements in the Bryansk district of the Russian Federation. In this area, which covers the two high contamination spots in the two countries following the accident, data on thyroid cancer incidence during the period 1991-1995 were analysed in the light of possible increased thyroid surveillance. Two methods of risk analysis were applied: Poisson regression with results for the single settlements and Monte Carlo (MC) calculations for results in larger areas or sub-populations. Best estimates of both methods agreed well. Poisson regression estimates of 95% confidence intervals (CIs) were considerably smaller than the MC results, which allow for extra-Poisson uncertainties due to reconstructed doses and the background thyroid cancer incidence. The excess absolute risk per unit thyroid dose (EARPD) for the birth cohort 1971-1985 by the MC analysis was 2.1 (95% CI 1.0-4.5) cases per 10(4) person-year Gy. The point estimate is lower by a factor of two than that observed in a pooled study of thyroid cancer risk after external exposures. The excess relative risk per unit thyroid dose was 23 (95% CI 8.6-82) Gy(-1). No significant differences between countries or cities and rural areas were found. In the lowest dose group of the settlements with an average thyroid dose of 0.05 Gy the risk was statistically significantly elevated. Dependencies of risks on age-at-exposure and on gender are consistent with findings after external exposures

Oxidant-NO dependent gene regulation in dogs with type I diabetes: impact on cardiac function and metabolism

<p>Abstract</p> <p>Background</p> <p>The mechanisms responsible for the cardiovascular mortality in type I diabetes (DM) have not been defined completely. We have shown in conscious dogs with DM that: <it>1</it>) baseline coronary blood flow (CBF) was significantly decreased, <it>2</it>) endothelium-dependent (ACh) coronary vasodilation was impaired, and <it>3</it>) reflex cholinergic NO-dependent coronary vasodilation was selectively depressed. The most likely mechanism responsible for the depressed reflex cholinergic NO-dependent coronary vasodilation was the decreased bioactivity of NO from the vascular endothelium. The goal of this study was to investigate changes in cardiac gene expression in a canine model of alloxan-induced type 1 diabetes.</p> <p>Methods</p> <p>Mongrel dogs were chronically instrumented and the dogs were divided into two groups: one normal and the other diabetic. In the diabetic group, the dogs were injected with alloxan monohydrate (40-60 mg/kg iv) over 1 min. The global changes in cardiac gene expression in dogs with alloxan-induced diabetes were studied using Affymetrix Canine Array. Cardiac RNA was extracted from the control and DM (n = 4).</p> <p>Results</p> <p>The array data revealed that 797 genes were differentially expressed (P < 0.01; fold change of at least ±2). 150 genes were expressed at significantly greater levels in diabetic dogs and 647 were significantly reduced. There was no change in eNOS mRNA. There was up regulation of some components of the NADPH oxidase subunits (gp91 by 2.2 fold, P < 0.03), and down-regulation of SOD1 (3 fold, P < 0.001) and decrease (4 - 40 fold) in a large number of genes encoding mitochondrial enzymes. In addition, there was down-regulation of Ca²⁺cycling genes (ryanodine receptor; SERCA2 Calcium ATPase), structural proteins (actin alpha). Of particular interests are genes involved in glutathione metabolism (glutathione peroxidase 1, glutathione reductase and glutathione S-transferase), which were markedly down regulated.</p> <p>Conclusion</p> <p>our findings suggest that type I diabetes might have a direct effect on the heart by impairing NO bioavailability through oxidative stress and perhaps lipid peroxidases.</p