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The Finnish forest workers' trade union and employers' organizations signed their first wage agreement in 1957 and first collective labour agreement in 1962. Many other sectors had concluded such agreements years earlier. This article challenges the widely accepted idea that collective labour agreements were becoming ubiquitous in Finnish industrial relations soon after the Second World War. Forest workers were left out of this process, and up until the late 1950s their wages and working conditions were not determined by the labour market parties but by state authorities – the state legislated and regulated forestry wages. The explanation for the delayed development of labour market practices in this sector can be found in forest work itself as well as the state's active role. This work was, up until the 1960s, done mainly by small farmers who were reluctant to unionize and unable to otherwise promote their interests. The situation changed when professionalization made them more or less full-time forest workers who more often joined the union. At the same time, the state created organizations and institutions which encouraged labour market parties to cooperate. Their shared struggle against political interference pushed labour market parties towards collective bargaining. [ABSTRACT FROM PUBLISHER]

The serotonin receptor 5-HT ligand 4-[F]fluoro-N-[2-[1-(2-methoxyphenyl)-1-piperazinyl]ethyl-N-2-pyridinyl-benzamide ( p-[F]MPPF) was produced by a simplified method of Le Bars et al. Traditional oil bath heating was compared to microwave heating. Various radioanalytical methods, radio-Thin Layer Chromatography (TLC), High Pressure Liquid Chromatography (HPLC) and Mass Spectrometry (MS), were compared in the evaluation of the labelled product(s). The crude reaction mixture consisted of p-[F]MPPF and 2-4 radioactive by-products eluting after the product fraction, and the reverse-phase HPLC method failed occasionally to separate p-[F]MPPF from the radioactive by-product with close retention time. The heating method had no significant effect on the composition of labelled by-products. In LC-(ESI)-MS analysis of p-[F]MPPF the labelled product was identified with m/ z ratio of 435 ([M + H]). The other HPLC fractions were measured to have following m/ z ratios: (1) 327; 349; (675) (2) 402; 407/408; (791) and (3) 436, suggesting different kind of decomposition of the labelled product and/or the inactive precursor. The ion trap mass spectrometer was sufficient for the qualitative analysis of p-[F]MPPF. However, differentiation of by-products arising from the decomposition of p-[F]MPPF or from its precursor p-MPPNO proved to be challenging. [ABSTRACT FROM AUTHOR]

Drug metabolism can result in the formation of highly reactive metabolites that are known to play a role in toxicity resulting in a significant proportion of attrition during drug development and clinical use. Thus, the earlier such reactivity was detected, the better. This review summarizes our multi-year project, together with pertinent literature, to examine a battery of in vitro tests capable of detecting the formation of reactive metabolites. Principal prerequisites for such tests were delineated: chemicals known/not known to cause tissue injury and produce reactive metabolites, activation system (mainly human-derived), small- and large-molecular targets (small-molecular trappers, peptides, proteins), analytical techniques (mass spectrometry), and cellular toxicity biomarkers. The current status of in vitro tools to detect reactive intermediates is the following: 1. Small-molecular trapping agents such glutathione or cyanide detect the production of reactive species with high sensitivity by proper MS technique. However, it seems that also putative "negatives" give rise to corresponding adducts. 2. Results from peptide and dG (DNA targeting) trapper studies are generally in line with those of small-molecular trappers, although also important differences exist. These two trapping platforms do not overlap. 3. It is anticipated that the in vitro adduct studies could be fully interpreted only in conjunction with toxicity biomarker (such as the Nrf2 pathway) information from whole cells or tissues. However, while there are tools to characterize the chemical liability and there are correlation between individual/integrated endpoints and toxicity, there are still severe gaps in understanding the mechanisms behind the link between reactive metabolites and adverse effects.