Anton Leopold Ruprecht - a chemist, mineralogist, metallurgist and a distinguished personality of the chemical revolution in the 18th century

<p>Based on Empress Maria Theresa’s order (of December 13, 1762) the first higher school institution specialised in technical education in Europewith the Department of Chemistry, Mineralogy and Metallurgy was founded in Schemnitz (present-day Banská Štiavnica) in 1763. The efforts to educate highly qualified technicians in mining, metallurgy and related fields in Austria-Hungary was crowned by foundation of this school, which in 1770 (after establishment of the Department of Mathematics, Mechanics and Hydraulics, and the Department of Mining Art and Mining Law) changed its name to a loud-sounding <strong>the Mining and Forestry Academy</strong>. Within a relatively short time, the school achieved a European recognition also by its research activities. Its particular importance emerged from the application of new scientific knowledge and development of progressive technological methods performed due to research outcomes. The school was characterised by adopting experimental methods based on measuring and weighing, and thus contributed significantly to revolutionary changes of scientific understanding of chemical processes, to supporting of Lavoisier’s oxidation theory and to discarding of the phlogiston interpretation of combustion. In the rich history of the Mining Academy since its foundation, the top positions were held by eminent and internationally recognized authorities who provided not only theoretical and practical teaching and training, but also research activities linked to the production practice – <strong>Nikolaus Joseph von Jacquin, Giovanni Antonio Scopoli, and particularly</strong> <strong>Anton Leopold von Ruprecht </strong>(1 – 10).</p>

Control of food intake by metabolism of fuels: a comparison across species

Research with laboratory species suggests that meals can be terminated by peripheral signals carried to brain feeding centres via hepatic vagal afferents, and that these signals are affected by oxidation of fuels. Pre-gastric fermentation in ruminants greatly alters fuels, allowing mechanisms conserved across species to be studied with different types and temporal absorption of fuels. These fuels include SCFA, glucose, lactate, amino acids and long-chain fatty acid (FA) isomers, all of which are absorbed and metabolised by different tissues at different rates. Propionate is produced by rumen microbes, absorbed within the timeframe of meals, and quickly cleared by the liver. Its hypophagic effects are variable, likely due to its fate; propionate is utilised for gluconeogenesis or oxidised and also stimulates oxidation of acetyl-CoA by anapleurosis. In contrast, acetate has little effect on food intake, likely because its uptake by the ruminant liver is negligible. Glucose is hypophagic in non-ruminants but not ruminants and unlike non-ruminant species, uptake of glucose by ruminant liver is negligible, consistent with the differences in hypophagic effects between them. Inhibition of FA oxidation increases food intake, whereas promotion of FA oxidation suppresses food intake. Hypophagic effects of fuel oxidation also vary with changes in metabolic state. The objective of this paper is to compare the type and utilisation of fuels and their effects on feeding across species. We believe that the hepatic oxidation theory allows insight into mechanisms controlling feeding behaviour that can be used to formulate diets to optimise energy balance in multiple species.

Diffusion in Internal Oxidation Reactions

When an alloy component is selectively oxidised but cannot reach the surface quickly enough to form a scale, then internal oxidation results. In this process, a gas phase oxidant dissolves in an alloy and diffuses inwards, reacting with a dilute solute metal to precipitate metal oxide or carbide, etc. Penetration kinetics are parabolic, the rate being controlled by oxidant diffusion and the concentration of reacting metal. Rates are predicted from classical oxidation theory on the basis that the reaction product is exceedingly stable, no solute metal remains in the reacted alloy, and oxidant diffusion is via a solvent metal matrix. This paper is concerned with situations where these approximations fail: the development of low stability precipitates and the growth of elongated precipitates which allow interfacial diffusion of the oxidant. Effects on the rates of internal oxidation are discussed.

High Temperature Oxidation of Liquid Cu-Ti Alloy at 1473K

The kinetics of oxidation of liquid Cu-0.5mass%Ti alloy at 1473K in CO2-CO gas mixture has been investigated by varying the oxygen potential. The pO2 is set to be enough to oxidize Ti in liquid Cu-Ti alloy but not for the oxidation of liquid Cu. Alloy samples were taken with a quartz tube during the experiments and Ti and O contents in the samples were analyzed by inductively coupled plasma method, and infrared absorption method. The phases of the formed titanium oxide layers were consisted of several different titanium oxides and were identified by using EBSD. The oxidation rate was evaluated based on the change of the Ti content in the Cu-Ti melts. The apparent overall oxidation rate is reasonably represented by the parabolic rate law. This oxidation behaviour was well explained based on the multi-layered oxidation theory.

Triggering of inflammatory response by myeloperoxidase-oxidized LDLAn oral presentation of the data was given before the Congress of the Beligian Society of Internal Medicine.

The oxidation theory proposes that LDL oxidation is an early event in atherosclerosis and that oxidized LDL contributes to atherogenesis in triggering inflammation. In contrast to the copper-modified LDL, there are few studies using myeloperoxidase-modified LDL (Mox-LDL) as an inflammation inducer. Our aim is to test whether Mox-LDL could constitute a specific inducer of the inflammatory response. Albumin, which is the most abundant protein in plasma and which is present to an identical concentration of LDL in the intima, was used for comparison. The secretion of IL-8 by endothelial cells (Ea.hy926) and TNF-α by monocytes (THP-1) was measured in the cell medium after exposure of these cells to native LDL, native albumin, Mox-LDL, or Mox-albumin. We observed that Mox-LDL induced a 1.5- and 2-fold increase (ANOVA; P < 0.001) in IL-8 production at 100 µg/mL and 200 µg/mL, respectively. The incubation of THP-1 cells with Mox-LDL (100 µg/mL) increased the production of TNF-α 2-fold over the control. Native LDL, albumin, and Mox-albumin showed no effect in either cellular types. The myeloperoxidase-modified LDL increase in cytokine release by endothelial and monocyte cells and by firing both local and systemic inflammation could induce atherogenesis and its development.

Lipid oxidation in atherogenesis: an overview

The ‘oxidation theory’ for atherosclerosis proposes that lipid and/or protein oxidation products are responsible for lesion formation/development. The major target for oxidation is suggested to be intimal low-density lipoprotein. This idea was stimulated by the pro-atherogenic properties of in vitro oxidized lipoproteins, such as stimulation of chemotaxis and sterol accumulation in macrophages, adhesion molecule expression on endothelial cells and apoptosis of several cell types. It was supported by detection of oxidation products in lesion lipoproteins, although these are (in general) less heavily oxidized and their biological activity is less rigorously defined than for their in vitro oxidized counterparts. Lesion lipids contain products generated by both enzymic and non-enzymic oxidation reactions; the majority are generated non-enzymically. The type and source of oxidant involved has been the subject of much speculation and is not resolved. The oxidation theory predicts that appropriate antioxidants will protect against atherosclerosis. Vitamin E has been used in several animal and human studies, but to date has shown little evidence of anti-atherosclerotic potential. However, lack of knowledge of the oxidant(s) driving lesion oxidation and the complexity of the anti- and pro-oxidant properties of vitamin E may explain its disappointing track record to date. These subjects require more rigorous study before the oxidation theory can be fairly tested.