Disposable optical sensor for Al(III) ions determination by coupled colorimetric solid-phase extraction-reflectance spectroscopy in leachates from cookware, antacids and hygienic care products.

A disposable and miniaturised optical sensor based on colorimetric solid-phase extraction has been designed using poly(styrene-divinylbenzene) membrane disks modified with the colorimetric reagent pyridoxal salicyloylhydrazone to determine the aluminium concentration in aqueous solutions. The extraction of Al(III) ions by the reagent immobilised onto a disk allows the quantification directly on the adsorbent surface by a miniature portable reflectance spectrometer with an optical fibre at 434 nm. The optimisation of the sensing system was carried out by a fractional factorial design 33-1 considering the extraction pH, amount of ligand immobilised onto the disk and time of immobilisation as experimental factors. The linear dynamic range of the sensor response ranged from 0.18 to 2 mg L-1 Al(III) with a detection limit of 0.18 mg L-1 (n = 10), being the precision of 6.3% for 1 mg L-1 Al(III) (n = 10, confidence level of 95%). The proposed method was successfully applied to the analysis of aluminium in leachates from cookware, antacids and hygienic care products, as contribution to the concern about aluminium as a known systemic toxicant at high doses.

Variant form of STAT4 is associated with primary Sjögren's syndrome.

Single nucleotide polymorphisms in the STAT4 gene have recently been shown to be associated with rheumatoid arthritis (RA) and systemic lupus erythematosus (SLE). Primary Sjögren's syndrome (pSS) is a related autoimmune disease thought to have a pathogenesis similar to these diseases. To test the hypothesis that the variant haplotype of STAT4 seen in RA and SLE is also associated with pSS, we genotyped rs7574865, the most strongly disease-associated SNP in the variant STAT4 haplotype, in 124 Caucasian pSS subjects and compared them to 1143 Caucasian controls. The disease-associated T allele was more common in chromosomes of the pSS patients (29.6%) than in controls (22.3%), leading to a P-value for association of 0.01. These results implicate polymorphisms in the STAT4 gene in the pathogenesis of pSS.