Influence of sodium dodecyl sulphate micelles on the kinetics of complex formation between Pd(H2O)(4)(2+) and S-carboxymethyl-L-cysteine

The kinetics of complex Formation between Pd(H(2)0)(4)(2+) and S-carboxymethyl-L-cysteine (SCMCH(2)) was investigated in the presence of sodium dodecyl sulphate in the acidity range between 2 M HClO4 and pH 5. Although the mechanism was not affected by the presence of anionic micelles, retardation (2.2 LT pH LT 5) and acceleration (pH LT 2.2) of the complex formation were observed compared with its rate in aqueous solution. These effects were interpreted in terms of the long-range electrostatic interactions between the negatively charged micellar surface and ligand species which can be in different ionic forms depending on the pH.5th European Symposium on Organic Reactivity (ESORV), Jul, 1995, Santiago Composte, Spai

Influence of sodium dodecyl sulfate micelles on the kinetics of complex formation between Pd(H2O)(4)(2+) and glutathione

The kinetics of the complex formation between Pd(H2O)(4)(2+) and glutathione was investigated in the presence of sodium dodecyl sulfate in the acidity range from 2 M HClO4 to pH 5. Acceleration (from 2 M HClO4 to pH 3.5) and retardation (3.5 LT pH LT 5) of the complex formation in the presence of anionic micelles was observed compared with the kinetic data in aqueous solution. These effects were explained by the electrostatic interaction of the reacting species with negatively charged micellar surface and their effective concentration and/or separation in the vicinity of micellar surface. Copyright (C) 1997 Elsevier Science Ltd

Kinetics of chelate formation between Pd-II and S-carboxymethyl-L-cysteine

The kinetics of the complex formation between S-carboxymethyl-L-cysteine and palladium(II) was studied by using stopped-flow technique in the acidity range from pH 1 to 4 at 25 degrees C. The reaction rate of the formation of 1 : 1 chelate species is strongly affected by the acidity. The reaction mechanism consisting of five parallel paths which involve Pd2+ and PdOH+, as well as LH-, LH2 and LH3+ ligand species was proposed. Fairly good agreement between the computed and experimentally determined rate constants was found. The equilibrium constants of the complex formation were determined. (C) 1998 Elsevier Science Ltd. All rights reserved

Altered glycogen metabolism in cultured astrocytes from mice with chronic glutathione deficit; relevance for neuroenergetics in schizophrenia.

Neurodegenerative and psychiatric disorders including Alzheimer's, Parkinson's or Huntington's diseases and schizophrenia have been associated with a deficit in glutathione (GSH). In particular, a polymorphism in the gene of glutamate cysteine ligase modulatory subunit (GCLM) is associated with schizophrenia. GSH is the most important intracellular antioxidant and is necessary for the removal of reactive by-products generated by the utilization of glucose for energy supply. Furthermore, glucose metabolism through the pentose phosphate pathway is a major source of NADPH, the cofactor necessary for the regeneration of reduced glutathione. This study aims at investigating glucose metabolism in cultured astrocytes from GCLM knockout mice, which show decreased GSH levels. No difference in the basal metabolism of glucose was observed between wild-type and knockout cells. In contrast, glycogen levels were lower and its turnover was higher in knockout astrocytes. These changes were accompanied by a decrease in the expression of the genes involved in its synthesis and degradation, including the protein targeting to glycogen. During an oxidative challenge induced by tert-Butylhydroperoxide, wild-type cells increased their glycogen mobilization and glucose uptake. However, knockout astrocytes were unable to mobilize glycogen following the same stress and they could increase their glucose utilization only following a major oxidative insult. Altogether, these results show that glucose metabolism and glycogen utilization are dysregulated in astrocytes showing a chronic deficit in GSH, suggesting that alterations of a fundamental aspect of brain energy metabolism is caused by GSH deficit and may therefore be relevant to metabolic dysfunctions observed in schizophrenia

Joint and several liability of the investor and general contractor for consideration due to the subcontractors after the changes introduced by the Act of 7 April 2017

Publikacja recenzowana / Peer-reviewed publicationPublikacja dotyczy niezmiernie istotnego z punktu widzenia praktyki budowlanej zagadnienia odpowiedzialności solidarnej inwestora i generalnego wykonawcy za zapłatę wynagrodzenia należnego podwykonawcy. Analizą objęte zostały nowe rozwiązania prawne, które wprowadzono ustawą z dnia 7 kwietnia 2017 r. o zmianie niektórych ustaw w celu ułatwienia dochodzenia wierzytelności. Na pierwszy rzut oka wydaje się, że rozstrzygają one wszelkie wątpliwości, jakie pojawiały się na gruncie wykładni art. 6471 k.c. Wnikliwa lektura rzeczonego przepisu prawnego pozwala stwierdzić, że jest to mylne odczucie.Th is article considers the problem of joint and several liability of the investor and general contractor for consideration due to the subcontractors what is an extremely principal issue from the point of view of construction industry. Th e analysis includes the new legal solutions which were introduced by the Act of 7 April 2017 about the changes of some acts to facilitate debt recovery. It seems at fi rst sight that the mentioned changes solve any kind of doubt which existed on basis of the interpretation of the Article 6471 of the Civil Code. A thorough reading of the said legal provision leads to a conclusion that it might be a confusing impression