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Incubating Hep G2 cells for 18 h with triparanol, buthiobate and low concentrations (< 0.5 /uM) of U18666A, inhibitors of desmosterol A24-reductase, of lanosterol l4x-demethylase and of squalene-2,3-epoxide cyclase (EC 5.4.99.7) respectively, resulted in a decrease of the HMG-CoA (3-hydroxy-3-methylglutaryl-coenzyme A) reductase activity. However, U18666A at concentrations higher than 3/tM increased the HMG-CoA reductase activity in a concentration-dependent manner. None of these inhibitors influenced directly the reductase activity in Hep G2 cell homogenates. Analysis by t.l.c. of 14C-labelled non-saponifiable lipids formed from either [14C]acetate or [14C]mevalonate during the cell incubations confirmed the sites of action of the drugs used. Beside the 14C-labelled substrates of the blocked enzymes and 14C-labelled cholesterol, another non-saponifiable lipid fraction was observed, which behaves as polar sterols on t.l.c. This was the case with triparanol and at those concentrations of U18666A that decreased the reductase activity, suggesting that polar sterols may play a role in suppressing the reductase activity.In the presence of 30/SM-Ut8666A (sterol formation blocked) the increase produced by simultaneously added compactin could be prevented by addition of mevalonate. This indicates the existence of a non-sterol mevalonate-derived effector in addition to a sterol-dependent regulation. LDL (low-density lipoprotein), which was shown to be able to decrease the compactin-induced increase in reductase activity, could not prevent the U18666A-induced increase. On the contrary, LDL enhanced the U18666A effect, showing that the LDL regulation is not merely the result of introducing cholesterol to the cells.

Transfer from a low cholesterol commercial diet to a high cholesterol diet, containing 2% (wt/wt) cholesterol and 0.5% cholate, caused an increase in serum cholesterol from about 2.5 mmol/L in two inbred rat strains to 5 mmol/L in the hyporesponsive strain and to 20 mmol/L in the hyperresponsive strain. In both strains the excess of cholesterol in the serum was exclusively located in the very low density lipoproteins. Cholesterol feeding caused a sevenfold increase in the amount of cholesterol in the liver, the increase tending to be greater in the hyporesponders. On the commercial diet, the decay of specific radioactivity of serum cholesterol after the intravenous administration of labeled cholesterol was faster in the hyporesponsive rats. The rate of fecal excretion of radioactive bile acids on this diet was higher in the hyporesponders when compared with the hyperresponders, whereas there was no strain difference with regard to the output of fecal neutral steroids. Sterol balance data showed that whole-body cholesterol synthesis on the low cholesterol diet was about twofold higher in the hypo- than in the hyperresponders. When fed the high cholesterol diet the half-life in the serum of injected radioactive cholesterol was about six times shorter in the hyporesponders. In absolute amounts, the hypo- and hyperresponders excreted similar amounts of endogenous (radioactive) bile acids and fecal steroids with the feces on this diet.

No abstract

We measured electron density and electron energy distribution function (EEDF) vertically through our reactor for a range of process conditions and for various gases. The EEDF of Ar plasma in the reactor could largely be described by the MaxwellBoltzmann distribution function, but it also contained a fraction (~10 -3 ) of electrons which were much faster (20-40 eV). At low pressures (6.8-11 µbar), the tail of fast electrons shifted to higher energies (E max ~ 50 eV) as we measured more towards the chuck. This tail of fast electrons could be shifted to lower energies (E max ~ 30 eV) when we increased pressure to 120 µbar or applied an external magnetic field of 9.5 µT. Addition of small amounts of N 2 (1-10%) or N 2 O (5%) to Ar plasma lowered the total density of slow electrons (approx. by a factor of two) but did not change the shape of the fast-electron tail of the EEDF. The ionization degree of Ar-plasma increased from 2.5·10 -4 to 5·10 -4 when an external magnetic field of 9.5 µT was applied. Motivation

Abstract-This paper presents a novel approach to make highperformance CMOS at low temperatures. Fully functional devices are manufactured using back-end compatible substrate temperatures after the deposition of the amorphous-silicon starting material. The amorphous silicon is pretextured to control the location of grain boundaries. Green-laser annealing is employed for crystallization and dopant activation.

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In this work, we emphasize the importance of using a correct Electron Energy Distribution Function (EEDF) to model chemical reactions in High-Density (HD) low-pressure silane-containing plasmas. We have modeled chemical reactions in Ar-SiH4-N2O-(N2-H2-O2) Inductively Coupled Plasma Enhanced Chemical Vapor Deposition (ICPECVD) system, intended for deposition of silicon oxide and silicon nitride layers. For the modeling, we used the experimentally measured EEDF, deviating from the Maxwell-Boltzmann (MB) EEDF. We demonstrate that the use of an inappropriate (i.e. MB in our example) EEDF, only slightly deviating from the experimental (i.e. actual) distribution, could lead to significant discrepancies (1-2 orders of magnitude) between the calculated and actual radical densities.