Synthesis of novel magnetic hydroxyapatite-biomass nanocomposite for arsenic and fluoride adsorption.

A magnetic nanocomposite of hydroxyapatite and biomass (HAp-CM) was synthesized through a combined ultrasonic and hydrothermal method, aiming for efficient adsorption of arsenic (As) and fluoride (F-) from drinking water in natural environments. The characterization of HAp-CM was carried out using TG, FTIR, XRD, SEM, SEM-EDS, and TEM techniques, along with the determination of pHpzc charge. FTIR analysis suggested that coordinating links are the main interactions that allow the formation of the nanocomposite. XRD data indicated that the crystalline structure of the constituent materials remained unaffected during the formation of HAp-CM. SEM-EDS analysis revelated a Ca/P molar ratio of 1.78. Adsorption assays conducted in batches demonstrated that As and F- followed a PSO kinetic model. Furthermore, As adsorption fitting well to the Langmuir model, while F- adsorption could be explained by both Langmuir and Freundlich models. The maximum adsorption capacity of HAp-CM was found to be 5.0 mg g-1 for As and 10.2 mg g-1 for F-. The influence of sorbent dosage, pH, and the presence of coexisting species on adsorption capacity was explored. The pH significantly affected the nanocomposite's efficiency in removing both pollutants. The presence of various coexisting species had different effects on F- removal efficiency, while As adsorption efficiency was generally enhanced, except in the case of PO43-. The competitive adsorption between F- and As on HAp-CM was also examined. The achieved results demonstrate that HAp-CM has great potential for use in a natural environment, particularly in groundwater remediation as a preliminary treatment for water consumption.

Tenascin-C degradation in chronic wounds is dependent on serine proteinase activity.

Degradation of extracellular matrix (ECM) components by proteinases is part of the physiological remodelling process during normal wound healing. Excessive degradation of the ECM, however, is likely to create an environment that can no longer support keratinocyte migration and is thought to play a role in the impaired healing of chronic ulcers. Tenascin-C is an ECM component that is markedly upregulated in acute and chronic wounds. Here we report on our investigations into the degradation of tenascin-C in chronic venous leg ulcers. We found proteolytic fragments of tenascin-C in leg ulcer exudate. We also detected fragments of fibronectin in the wound fluid and in addition observed breakdown of fibronectin by wound fluid in vitro, as has previously been reported by others. Wound fluid of four out of six chronic leg ulcers degraded purified human tenascin-C in vitro, and degradation of tenascin-C correlated with high levels of functionally active leucocyte elastase and metalloproteinases in the wound fluid. To identify which proteinases were involved in tenascin-C degradation, we tested the effect of specific proteinase inhibitors. The addition of EDTA or E64 did not protect tenascin-C from degradation, suggesting that neither metalloproteinases nor cysteine proteinases are responsible for cleavage. Tenascin-C breakdown was inhibited by PMSF and SKALP/elafin, and we therefore conclude that leucocyte elastase and possibly other serine proteinases are the tenascin-C-degrading enzymes in ulcer exudate. Taking into account the possible effects of tenascin-C and tenascin-C fragments on cell behaviour, we hypothesize that degradation of tenascin-C could affect the healing process in chronic venous ulcers.