Regulated Mycotoxin Occurrence and Co-Occurrence in Croatian Cereals

A total of 209 samples of various cereal crops (maize, wheat, barley, rye and oats) grown in Croatian fields during 2016 and 2017 were collected to analyze and determine the occurrence and co-occurrence of EU regulated mycotoxins in cereals (AFB1, AFB2, AFG1, AFG2, DON, FB1, FB2, ZEA, T-2, HT-2 and OTA). The analysis, performed by a validated confirmatory LC-MS/MS method based on a dilute and shoot principle, highlighted Fusarium mycotoxins as the main contaminants, often co-occurring in samples from both years (50.0% in 2016 and 33.7% in 2017). DON was found to be the most frequent mycotoxin, present in 72.5% of the 2016 samples and 32.6% of the 2017 samples, while maize proved to be the most contaminated cereal type of both years with FUM as the most abundant mycotoxins, with an average concentration of 1180 µg/kg. Moderate temperatures with periods of high humidity favored the accumulation of DON in wheat samples instead of other Fusarium mycotoxins, while similar conditions favored maize contamination with FUM. A total of 8.3% of all the 2016 harvest samples and 7.9% of the 2017 harvest samples were assessed as non-compliant, containing mycotoxins in concentrations higher than the levels set by the EU legislation for food.     

Gingival crevicular fluid and serum levels of APRIL,BAFF and TNF-alpha in rheumatoid arthritis and osteoporosis patients with periodontal disease

Background

This study was performed to evaluate gingival crevicular fluid (GCF) and serum levels of a proliferation inducing ligand (APRIL) and B cell activating factor (BAFF) and compare this to differences between TNF-alpha levels in rheumatoid arthritis (RA), osteoporosis (OPR) and systemically healthy women with periodontal disease (SH).

Design

Gingival crevicular fluid (GCF) and serum samples were obtained before any periodontal intervention from 17 RA, 19 OPR patients and 13 SH women with periodontitis. Full-mouth clinical periodontal measurements were recorded. APRIL, BAFF and TNF-α levels were determined by ELISA. Statistical analysis was performed using multivariate analysis, ANOVA and Spearman correlation.

Results

Pocket depths differed in site-specific comparisons, but otherwise clinical measurements were similar in the three study groups. Multivariate least squares regression ANOVA adjusted for age and for plaque index indicated that total amounts of TNF-α and concentrations of TNF-α, BAFF and APRIL were significantly greater in the RA patients than in the SH group (p < 0.05), and GCF concentrations of BAFF were greater in OPR patients than in SH. Serum TNF-α and BAFF were significantly higher in the RA group compared to SH (p < 0.05) and serum TNF-α was greater in RA than in OPR (p < 0.05). APRIL and BAFF correlated with RANKL levels in GCF and serum (p < 0.05).

Conclusion

Despite long-term usage of anti-inflammatory drugs in the RA and OPR patients, increased TNF-family cytokines, might suggest that these patients have a propensity to overproduce these inflammatory mediators but whether this results from greater disease activity or contribute to greater disease activity remains moot.     

Work-Induced potassium changes in muscle venous effluent blood measured by ion-specific electrodes

Summary Modified Walker's liquid ion-exchanger microelectrodes were employed for measuring changes of K⁺ concentration in venous effluent blood from the cat gastrocnemius muscle during and after isometric tetani of various duration induced by indirect stimulation. The time course of these changes was obtained and the overall loss of K⁺ from a working muscle could thus be estimated. By comparing present results in the venous blood and previous findings of K⁺ concentration changes in the muscle extracellular space, a concentration gradient was found between the muscle and venous effluent blood.The authors wish to acknowledge the assistance of Dr. J. L. Walker in developing the ion-specific microelectrodes and for supplying them with silicone oil and Corning ion-exchanger.     

Hybrid compound based on diethylenetriaminecopper(ii) cations and scarce V-monosubstituted β-octamolybdate as water oxidation catalyst

Herein, we report on a new hybrid compound (NH₄){[Cu(dien)(H₂O)₂]₂[β-VMo₇O₂₆]}·1.5H₂O (1), where dien = diethylenetriamine, containing an extremely rare mixed-metal pseudo-octamolybdate cluster. An ex situ EPR spectroscopy provided insights into the formation of paramagnetic species in reaction mixture and in solution of 1. The magneto-structural correlations revealed weak antiferromagnetic exchange interactions between the [Cu(dien)]²⁺ cations transmitted by intermolecular pathways. The cyclic voltammetry showed the one-electron process associated with the Cu³⁺/Cu²⁺ oxidation followed by the multi-electron catalytic wave due to water oxidation with a faradaic yield of 86%. The title compound was thus employed in homogeneous water oxidation catalysis using tris(bipyridine)ruthenium photosensitizer. At pH 8.0, efficiency of the catalytic system attained 0.19 turnovers per second supported by the relatively mild water oxidation overpotential of 0.54 V.

A new hybrid compound (NH₄){[Cu(dien)(H₂O)₂]₂[β-VMo₇O₂₆]}·1.5H₂O was employed in homogeneous water oxidation catalysis. At pH 8.0, its efficiency attains 0.19 turnovers per second, supported by the relatively mild water oxidation overpotential of 0.54 V.     

Reduction of soluble adhesion molecules (sICAM-1, sVCAM-1, and sE-selectin) and vascular endothelial growth factor levels in serum of rheumatoid arthritis patients following multiple intravenous infusions of infliximab

INTRODUCTION: The purpose of this study was to determine the effect of repeated infusions of infliximab, a chimeric anti-tumor necrosis factor (anti-TNF)-alpha antibody, on the levels of soluble adhesion molecules and vascular endothelial growth factor (VEGF) in patients with active rheumatoid arthritis (RA). MATERIALS AND METHODS: The treatment design consisted of 9 infusions of infliximab (3 mg/kg) at weeks 0, 2, 6, and every 8 weeks thereafter. All patients had been receiving methotrexate (MTX; 7.5-20 mg/week). Serum levels of soluble intercellular adhesion molecule (sICAM)-1, vascular cell adhesion molecule (sVCAM)-1, E-selectin (sE-selectin), and VEGF were measured by ELISA at weeks 0, 2, 6, 14, and 38 prior to infusion, and at week 62. RESULTS: A remarkable decrease in serum sICAM-1 (p<0.001), sVCAM-1 (p<0.01), sE-selectin (p<0.01) and VEGF (p<0.001) levels was observed in RA patients after the initial dose of infliximab. The second administration of the drug was followed by an even more significant suppression of serum sICAM-1, sVCAM-1, sE-selectin, and VEGF (p<0.001 in all cases). Further infliximab infusions also significantly reduced serum soluble adhesion molecules and VEGF concentrations, although these were less effective. Infliximab treatment induced a significant decrease in the number of monocytes observed until the end of the study. CONCLUSIONS: Our study, besides a rapid suppression of disease activity, showed that serum soluble adhesion molecules and VEGF concentrations are down-regulated following anti-TNF-alpha antibody therapy combined with MTX. Repeated doses of infliximab sustained the reductions in the soluble adhesion molecules and VEGF concentrations, although they were less effective than the first and second infusions of infliximab.     

Predominance of null mutations in ataxia-telangiectasia

Ataxia-telangiectasia (A-T) is an autosomal recessive disorder involving cerebellar degeneration, immunodeficiency, chromosomal instability, radiosensitivity and cancer predisposition. The responsible gene, ATM, was recently identified by positional cloning and found to encode a putative 350 kDa protein with a Pl 3-kinase-like domain, presumably involved in mediating cell cycle arrest in response to radiation-induced DNA damage. The nature and location of A-T mutations should provide insight into the function of the ATM protein and the molecular basis of this pleiotropic disease. Of 44 A-T mutations identified by us to date, 39 (89%) are expected to inactivate the ATM protein by truncating it, by abolishing correct initiation or termination of translation, or by deleting large segments. Additional mutations are four smaller in-frame deletions and insertions, and one substitution of a highly conserved amino acid at the Pl 3-kinase domain. The emerging profile of mutations causing A-T is thus dominated by those expected to completely inactivate the ATM protein. ATM mutations with milder effects may result in phenotypes related, but not identical, to A-T.