Surface cellulose modification with 2-aminomethylpyridine for copper, cobalt, nickel and zinc removal from aqueous solution

Cellulose was first modified with thionyl chloride, followed by reaction with 2-aminomethylpyridine to yield 6-(2'-aminomethylpyridine)-6-deoxycellulose. The resulting chemically-immobilized surface was characterized by elemental analysis, FTIR, 13C NMR and thermogravimetry. From 0.28% of nitrogen incorporated in the polysaccharide backbone, the amount of 0.10 ± 0.01 mmol of the proposed molecule was anchored per gram of the chemically modified cellulose. The available basic nitrogen centers attached to the covalent pendant chain bonded to the biopolymer skeleton were investigated for copper, cobalt, nickel and zinc adsorption from aqueous solution at room temperature. The newly synthesized biopolymer gave maximum sorption capacities of 0.100 ± 0.012, 0.093 ± 0.021, 0.074 ± 0.011 and 0.071 ± 0.019 mmol.g-1 for copper, cobalt, nickel and zinc cations, respectively, using the batchwise method, whose data was fitted to different sorption models, the best fit being obtained with the Langmuir model. The results suggested the use of this anchored biopolymer for cation removal from the environment

Inflammatory mechanisms in tendinopathy - towards translation

Tendinopathy is a multifactorial spectrum of tendon disorders that affects different anatomical sites and is characterized by activity-related tendon pain. These disorders are common, account for a high proportion (~30%) of referrals to musculoskeletal practitioners and confer a large socioeconomic burden of disease. Our incomplete understanding of the mechanisms underpinning tendon pathophysiology continues to hamper the development of targeted therapies, which have been successful in other areas of musculoskeletal medicine. Debate remains among clinicians about the role of an inflammatory process in tendinopathy owing to a lack of clinical correlation. The advent of modern molecular techniques has highlighted the presence of immune cells and inflammatory mechanisms throughout the spectrum of tendinopathy in both animal and human models of disease. Key inflammatory mediators — such as cytokines, nitric oxide, prostaglandins and lipoxins — play crucial parts in modulating changes in the extracellular matrix within tendinopathy. Understanding the links between inflammatory mechanisms, tendon homeostasis and resolution of tendon damage will be crucial in developing novel therapeutics for human tendon disease