Determination of resin acids in pulp mill EOP bleaching process effluent

Resin acids are tricyclic diterpenoids which are natural constituents of the wood from conifers. They are released from the wood during the manufacture of pulp and paper. These acids are very resistant to chemical degradation and survive the pulping and also the EOP bleaching process (EOP=alkaline extraction, oxygen and peroxide, the chemicals used in the bleaching process). Resin acids were extracted from alkaline medium using liquid–liquid extraction with t-butyl methyl ether and solid phase extraction with RP C18 adsorbent and a highly porous polystyrene-divinylbenzene polymer. After conversion of the acids to their pentafluorobenzyl esters, the extracts were analysed by GC/MS using a 25 m OV17 capillary column. Recovery values for single resin acids were determined by all three extraction methods. The solid phase extraction methods were applied to the analysis of the EOP effluent from a pulp mill bleaching process. 14 different resin acids and one resin acid methyl ester have been identified in the effluent. One of these was an oxo resin acid which might well be a product of the bleaching process.     

The Chemistry and Biology of Soluble Guanylate Cyclase Stimulators and Activators

The vasodilatory properties of nitric oxide (NO) have been utilized in pharmacotherapy for more than 130 years. Still today, NO‐donor drugs are important in the management of cardiovascular diseases. However, inhaled NO or drugs releasing NO and organic nitrates are associated with noteworthy therapeutic shortcomings, including resistance to NO in some disease states, the development of tolerance during long‐term treatment, and nonspecific effects, such as post‐translational modification of proteins. The beneficial actions of NO are mediated by stimulation of soluble guanylate cyclase (sGC), a heme‐containing enzyme which produces the intracellular signaling molecule cyclic guanosine monophosphate (cGMP). Recently, two classes of compounds have been discovered that amplify the function of sGC in a NO‐independent manner, the so‐called sGC stimulators and sGC activators. The most advanced drug, the sGC stimulator riociguat, has successfully undergone Phase III clinical trials for different forms of pulmonary hypertension.