The most common method to measure direct current high voltage (HV) down to the ppm-level is to use resistive high-voltage dividers. Such devices scale the HV into a range where it can be compared ...with precision digital voltmeters to reference voltages sources, which can be traced back to Josephson voltage standards. So far the calibration of the scale factors of HV dividers for voltages above 1 kV could only be done at metrology institutes and sometimes involves round-robin tests among several institutions to get reliable results. Here we present a novel absolute calibration method based on the measurement of a differential scale factor, which can be performed with commercial equipment and outside metrology institutes. We demonstrate that reproducible measurements up to 35 kV can be performed with relative uncertainties below . This method is not restricted to metrology institutes and offers the possibility to determine the linearity of high-voltage dividers for a wide range of applications.
We hypothesized that the lipid-activated transcription factor, the peroxisome proliferator-activated receptor α (PPARα), plays a pivotal role in the cellular metabolic response to fasting. Short-term ...starvation caused hepatic steatosis, myocardial lipid accumulation, and hypoglycemia, with an inadequate ketogenic response in adult mice lacking PPARα (PPARα -/-), a phenotype that bears remarkable similarity to that of humans with genetic defects in mitochondrial fatty acid oxidation enzymes. In PPARα +/+ mice, fasting induced the hepatic and cardiac expression of PPARα target genes encoding key mitochondrial (medium-chain acyl-CoA dehydrogenase, carnitine palmitoyltransferase I) and extramitochondrial (acyl-CoA oxidase, cytochrome P450 4A3) enzymes. In striking contrast, the hepatic and cardiac expression of most PPARα target genes was not induced by fasting in PPARα -/- mice. These results define a critical role for PPARα in a transcriptional regulatory response to fasting and identify the PPARα -/- mouse as a potentially useful murine model of inborn and acquired abnormalities of human fatty acid utilization.
The peroxisome proliferator-activated receptor alpha (PPARalpha) is a nuclear receptor implicated in the control of cellular lipid utilization. To test the hypothesis that PPARalpha is activated as a ...component of the cellular lipid homeostatic response, the expression of PPARalpha target genes was characterized in response to a perturbation in cellular lipid oxidative flux caused by pharmacologic inhibition of mitochondrial fatty acid import. Inhibition of fatty acid oxidative flux caused a feedback induction of PPARalpha target genes encoding fatty acid oxidation enzymes in liver and heart. In mice lacking PPARalpha (PPARalpha-/-), inhibition of cellular fatty acid flux caused massive hepatic and cardiac lipid accumulation, hypoglycemia, and death in 100% of male, but only 25% of female PPARalpha-/- mice. The metabolic phenotype of male PPARalpha-/- mice was rescued by a 2-wk pretreatment with beta-estradiol. These results demonstrate a pivotal role for PPARalpha in lipid and glucose homeostasis in vivo and implicate estrogen signaling pathways in the regulation of cardiac and hepatic lipid metabolism.
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