Palladium nanoparticles on InP for hydrogen detection

Layers of palladium (Pd) nanoparticles on indium phosphide (InP) were prepared by electrophoretic deposition from the colloid solution of Pd nanoparticles. Layers prepared by an opposite polarity of deposition showed different physical and morphological properties. Particles in solution are separated and, after deposition onto the InP surface, they form small aggregates. The size of the aggregates is dependent on the time of deposition. If the aggregates are small, the layer has no lateral conductance. Forward and reverse I-V characteristics showed a high rectification ratio with a high Schottky barrier height. The response of the structure on the presence of hydrogen was monitored

Layers of Metal Nanoparticles on Semiconductors Deposited by Electrophoresis from Solutions with Reverse Micelles

Pd nanoparticles were prepared with reverse micelles of water/AOT/isooctane solution and deposited onto silicon or InP substrates by electrophoresis. A large change of capacitance-voltage characteristics of mercury contacts on a semiconductor was found after Pd deposition. This change could be modified when the Pd deposition is followed by a partial removal of the deposited AOT. The deposited Pd nanoparticles were investigated by optical mictroscopy, SIMS and SEM. Finally, Schottky diodes with barrier height as high as 1.07 eV were prepared by deposition of Pd nanoparticles on n-type InP and by a partial removal of superfluous AOT. These diodes are prospective structures for further testing as hydrogen sensors

ATP synthase: from single molecule to human bioenergetics

ATP synthase (FoF1) consists of an ATP-driven motor (F1) and a H+-driven motor (Fo), which rotate in opposite directions. FoF1 reconstituted into a lipid membrane is capable of ATP synthesis driven by H+ flux. As the basic structures of F1 (α3β3γδε) and Fo (ab2c10) are ubiquitous, stable thermophilic FoF1 (TFoF1) has been used to elucidate molecular mechanisms, while human F1Fo (HF1Fo) has been used to study biomedical significance. Among F1s, only thermophilic F1 (TF1) can be analyzed simultaneously by reconstitution, crystallography, mutagenesis and nanotechnology for torque-driven ATP synthesis using elastic coupling mechanisms. In contrast to the single operon of TFoF1, HFoF1 is encoded by both nuclear DNA with introns and mitochondrial DNA. The regulatory mechanism, tissue specificity and physiopathology of HFoF1 were elucidated by proteomics, RNA interference, cytoplasts and transgenic mice. The ATP synthesized daily by HFoF1 is in the order of tens of kilograms, and is primarily controlled by the brain in response to fluctuations in activity

Lower Fasting Muscle Mitochondrial Activity Relates to Hepatic Steatosis in Humans

OBJECTIVE Muscle insulin resistance has been implicated in the development of steatosis and dyslipidemia by changing the partitioning of postprandial substrate fluxes. Also, insulin resistance may be due to reduced mitochondrial function. We examined the association between mitochondrial activity, insulin sensitivity, and steatosis in a larger human population. RESEARCH DESIGN AND METHODS We analyzed muscle mitochondrial activity from ATP synthase flux (fATP) and ectopic lipids by multinuclei magnetic resonance spectroscopy from 113 volunteers with and without diabetes. Insulin sensitivity was assessed from M values using euglycemic-hyperinsulinemic clamps and/or from oral glucose insulin sensitivity (OGIS) using oral glucose tolerance tests. RESULTS Muscle fATP correlated negatively with hepatic lipid content and HbA1c. After model adjustment for study effects and other confounders, fATP showed a strong negative correlation with hepatic lipid content and a positive correlation with insulin sensitivity and fasting C-peptide. The negative correlation of muscle fATP with age, HbA1c, and plasma free fatty acids was weakened after adjustment. Body mass, muscle lipid contents, plasma lipoproteins, and triglycerides did not associate with fATP. CONCLUSIONS The association of impaired muscle mitochondrial activity with hepatic steatosis supports the concept of a close link between altered muscle and liver energy metabolism as early abnormalities promoting insulin resistance