Seasonality in the relationship between equatorial-mean heat content and interannual eastern equatorial Atlantic sea surface temperature variability.

Interannual sea surface temperature (SST) variations in the tropical Atlantic Ocean lead to anomalous atmospheric circulation and precipitation patterns with important ecological and socioeconomic consequences for the semiarid regions of sub-Saharan Africa and northeast Brazil. This interannual SST variability is characterized by three modes: an Atlantic meridional mode featuring an anomalous cross-equatorial SST gradient that peaks in boreal spring; an Atlantic zonal mode (Atlantic Niño mode) with SST anomalies in the eastern equatorial Atlantic cold tongue region that peaks in boreal summer; and a second zonal mode of variability with eastern equatorial SST anomalies peaking in boreal winter. Here we investigate the extent to which there is any seasonality in the relationship between equatorial warm water recharge and the development of eastern equatorial Atlantic SST anomalies.

Gate Spacer Investigation for Improving the Speed of High-Frequency Carbon Nanotube-Based Field-Effect Transistors.

Carbon nanotube (CNT)-based field-effect transistors have demonstrated great potential for high-frequency (HF) analog transceiver electronics. Despite significant advancements, one of the remaining challenges is the optimization of the device architecture for obtaining the highest possible speed and linearity. While most studies so far have concentrated on symmetrical top gated FET devices, we report on the impact of the device architecture on their HF performance.

Polymer-based doping control for performance enhancement of wet-processed short-channel CNTFETs.

The electrical transport properties of short-channel transistors based on single-walled carbon nanotubes (CNT) are significantly affected by bundling along with solution processing. We report that especially high off currents of CNT transistors are not only related to the incorporation of metallic CNTs but also to the incorporation of CNT bundles. By applying device passivation with poly(4-vinylpyridine), the impact of CNT bundling on the device performance can be strongly reduced due to increased gate efficiency as well as reduced oxygen and water-induced p-type doping, boosting essential field-effect transistor performance parameters by several orders of magnitude.

Towards an optimal contact metal for CNTFETs.

Downscaling of the contact length Lc of a side-contacted carbon nanotube field-effect transistor (CNTFET) is challenging because of the rapidly increasing contact resistance as Lc falls below 20-50 nm. If in agreement with existing experimental results, theoretical work might answer the question, which metals yield the lowest CNT-metal contact resistance and what physical mechanisms govern the geometry dependence of the contact resistance. However, at the scale of 10 nm, parameter-free models of electron transport become computationally prohibitively expensive.

Microdialysis-based analysis of interstitial NO in situ: NO synthase-independent NO formation during myocardial ischemia.

Objectives: Nitric oxide (NO) synthesis by NO synthases (NOS) requires oxygen. However, although counterintuitive, NO synthesis is increased in ischemic myocardium. Accordingly, mechanisms independent of the NOS pathway have been suggested to contribute to NO synthesis during ischemia.

Inhibition of Na+/H+-exchanger with sabiporide attenuates the downregulation and uncoupling of the myocardial beta-adrenoceptor system in failing rabbit hearts.

Chronic heart failure (HF) is characterized by left ventricular (LV) structural remodeling, impaired function, increased circulating noradrenaline (NA) levels and impaired responsiveness of the myocardial beta-adrenoceptor (betaAR)-adenylyl cyclase (AC) system. In failing hearts, inhibition of the sodium/proton-exchanger (NHE)-1 attenuates LV remodeling and improves LV function. The mechanism(s) involved in these cardioprotective effects remain(s) unclear, but might involve effects on the impaired betaAR-AC system.

Preinfarction angina: no interference of coronary microembolization with acute ischemic preconditioning.

Transient episodes of angina preceding acute myocardial infarction may both, protect the myocardium by ischemic preconditioning or damage it when associated with coronary microembolization. We now studied the potential loss of ischemic preconditioning with coronary microembolization. Anesthetized pigs (group 1; n=8) were subjected to 90 min sustained low-flow ischemia.

Coronary microembolization does not induce acute preconditioning against infarction in pigs-the role of adenosine.

Objective: After coronary microembolization (ME) adenosine is released from ischemic areas of the microembolized myocardium. This adenosine dilates vessels in adjacent nonembolized myocardium and increases coronary blood flow. For ischemic preconditioning (IP) to protect the myocardium against infarction, an increase in the interstitial adenosine concentration (iADO) prior to the subsequent ischemia/reperfusion is necessary.

Serum but not myocardial TNF-alpha concentration is increased in pacing-induced heart failure in rabbits.

In animals and patients with severe heart failure (HF), the serum tumor necrosis factor-alpha (TNF-alpha) concentration is increased. It is, however, still controversial whether or not such increased serum TNF-alpha originates from the heart itself or is of peripheral origin secondary to gastrointestinal congestion and increased endotoxin concentration. We therefore now examined TNF-alpha in serum, myocardium, and liver of sham-operated and HF rabbits.

Effect of NO synthase inhibition on myocardial metabolism during moderate ischemia.

Nitric oxide (NO) is involved in the control of myocardial metabolism. In normoperfused myocardium, NO synthase inhibition shifts myocardial metabolism from free fatty acid (FFA) toward carbohydrate utilization. Ischemic myocardium is characterized by a similar shift toward preferential carbohydrate utilization, although NO synthesis is increased.

B-type natriuretic peptide limits infarct size in rat isolated hearts via KATP channel opening.

B-type natriuretic peptide (BNP) has been reported to be released from the myocardium during ischemia. We hypothesized that BNP mediates cardioprotection during ischemia-reperfusion and examined whether exogenous BNP limits myocardial infarction and the potential role of ATP-sensitive potassium (K(ATP)) channel opening. Langendorff-perfused rat hearts underwent 35 min of left coronary artery occlusion and 120 min of reperfusion.

Myocardial dysfunction with coronary microembolization: signal transduction through a sequence of nitric oxide, tumor necrosis factor-alpha, and sphingosine.

Coronary microembolization results in progressive myocardial dysfunction, with causal involvement of tumor necrosis factor-alpha (TNF-alpha). TNF-alpha uses a signal transduction involving nitric oxide (NO) and/or sphingosine. Therefore, we induced coronary microembolization in anesthetized dogs and studied the role and sequence of NO, TNF-alpha, and sphingosine for the evolving contractile dysfunction.