The electrochemical reduction of a cadmium cryptate on a mercury electrode in acetonitrile.

The reduction of the Cd(2,2,2)2+ complex has been studied in acetonitrile using polarography, chronocoulometry, and cyclic voltammetry. The corresponding kinetic parameters have been calculated and are compared with those obtained for the solvated cadmium cation in the same solvent. The study of the electrochemical reduction mechanism showed that the final stable products are the free ligand (2,2,2) and cadmium-amalgam. The stability constant of the cadmium cryptate in acetonitrile has been estimated as log Ks = 17.3 from the electrochemical measurements

Dimethylpropyleneurea-water mixtures .1. Physical-properties.

Densities, refractive indices, viscosities, dielectric constants and the absorptions of several solvatochromic indicators have been determined at 25°C for mixtures of N,N′-dimethyl-N,N′-propyleneurea (DMPU) and water in the complete mole fraction scale. the results are compared with the properties of hexamethylphosphotriamide (HMPT) and its mixtures with water which show a striking similarity to DMPU and its mixtures with water. Since HMPT was found to be carcinogenic in animal tests, DMPU offers a suitable substitute since it may be regarded as safe under laboratory conditions

Solvent dependence of kinetics and equilibria of thallium(I) cryptates in relation to the free energies of solvation of thallium(I).

Stability constants and dissociation rate constants of thallium (I) cryptates have been measured in several solvents at 25 °C. The Tl+ cryptates are more stable and less sensitive to ligand cavity size than the corresponding complexes of the alkali-metal cations. The stability constants vary strongly with solvent, and the solvent dependence of the complex stabilities appears to reflect mainly changes in the solvation of Tl+. It is shown that free energies of transfer of the solvated Tl+ among non–aqueous solvents calculated on the assumption that the difference in the free energies of transfer of the Tl+ cryptates and the corresponding cryptands is zero are in good agreement with literature data. Changes in the stability constants with solvent and ligand are reflected in changes in both dissociation and formation rate constants, but more so in the former. Thus the solvation of the transition state, (Tl+⋯Cry)[graphic omitted], is rather closer to that of the reactants, and includes additional solvent interactions compared with the stable cryptate complex, TlCry+

Report on the 2012 Proficiency Test on pyrrolizidine alkaloids in honey and hay

The purpose of this proficiency test was to investigate the current measurement capacities of testing laboratories for pyrrolizidine alkaloids in honey and plant materials. The scheme consisted of two parts: Benchmarking performance of laboratories against known estimates of pyrrolizidine alkaloids in the samples and checking for methodological differences while measuring naturally contaminated materials. Twenty-eight laboratories expressed their will to participate and analysed multiple analytes in several test samples of honey and plant material. The analysis of spiked honey showed no statistical differences between determining a common sum parameter for alkaloids and individual determination. A significant difference has been found however for of naturally contaminated materials. Individual alkaloid determination showed significantly lower results, possibly because of the presence of substances contributing to the sum parameter that were not in the scopes of the methods applied as well as lack of standard materials available on the market. Satisfactory performance for all of analytes has been achieved by more than half of participants analysing for both: sum parameter, and alkaloids analysed individually.JRC.D.5-Standards for Food Bioscienc

Rescue of DNA damage after constricted migration reveals a mechano-regulated threshold for cell cycle.

Migration through 3D constrictions can cause nuclear rupture and mislocalization of nuclear proteins, but damage to DNA remains uncertain, as does any effect on cell cycle. Here, myosin II inhibition rescues rupture and partially rescues the DNA damage marker γH2AX, but an apparent block in cell cycle appears unaffected. Co-overexpression of multiple DNA repair factors or antioxidant inhibition of break formation also exert partial effects, independently of rupture. Combined treatments completely rescue cell cycle suppression by DNA damage, revealing a sigmoidal dependence of cell cycle on excess DNA damage. Migration through custom-etched pores yields the same damage threshold, with ∼4-µm pores causing intermediate levels of both damage and cell cycle suppression. High curvature imposed rapidly by pores or probes or else by small micronuclei consistently associates nuclear rupture with dilution of stiff lamin-B filaments, loss of repair factors, and entry from cytoplasm of chromatin-binding cGAS (cyclic GMP-AMP synthase). The cell cycle block caused by constricted migration is nonetheless reversible, with a potential for DNA misrepair and genome variation

Comparison of urinary aflatoxin M1 and aflatoxin albumin adducts as biomarkers for assessing aflatoxin exposure in Tanzanian children

Purpose: To determine levels of urinary aflatoxin M1 (AFM1) in children and correlate the concentrations with previously reported aflatoxin albumin adduct (AF-alb) levels in these children. Materials and methods: Matched urine and blood samples were collected from 84 Tanzanian children aged 6–14 months old. From 31 children in one village (Kigwa), samples were collected at three time points six months apart. Samples were collected from 31 and 22 children from two different regions at the second time point only. Urinary AFM1 was measured using a commercial enzyme-linked immunosorbent assay (ELISA) kit with a modified protocol to improve sensitivity. AF-alb was measured using an established ELISA method. Results: The relative ranking of the three villages for exposure to aflatoxin based on either AFM1 or AF-alb biomarker measurements was the same. In Kigwa village, both AFM1 and AF-alb levels were higher at six months post-harvest compared to baseline. However, at the next visit, the AFM1 levels dropped from a GM (interquartile range) of 71.0 (44.7, 112.6) at visit two to 49.3 (31.5, 77.3) pg/ml urine, whereas AF-alb levels increased from 47.3 (29.7, 75.2) to 52.7 (35.4, 78.3) pg/mg albumin between these two visits, reflecting the fact that AFM1 measures short-term exposure, whereas AF-alb measures longer term exposure. There was a correlation between AFB1 intake and AFM1 excretion (r= 0.442, p ≤ 0.001). Conclusions: Urinary AFM1 is a good biomarker for AFB1 exposure in Tanzanian children, reflecting geographical and temporal variations in exposure to this foodborne toxin

Stimulatory MAIT cell antigens reach the circulation and are efficiently metabolised and presented by human liver cells.

OBJECTIVE Mucosal-associated invariant T (MAIT) cells are the most abundant T cells in human liver. They respond to bacterial metabolites presented by major histocompatibility complex-like molecule MR1. MAIT cells exert regulatory and antimicrobial functions and are implicated in liver fibrogenesis. It is not well understood which liver cells function as antigen (Ag)-presenting cells for MAIT cells, and under which conditions stimulatory Ags reach the circulation. DESIGN We used different types of primary human liver cells in Ag-presentation assays to blood-derived and liver-derived MAIT cells. We assessed MAIT cell stimulatory potential of serum from healthy subjects and patients with portal hypertension undergoing transjugular intrahepatic portosystemic shunt stent, and patients with inflammatory bowel disease (IBD). RESULTS MAIT cells were dispersed throughout healthy human liver and all tested liver cell types stimulated MAIT cells, hepatocytes being most efficient. MAIT cell activation by liver cells occurred in response to bacterial lysate and pure Ag, and was prevented by non-activating MR1 ligands. Serum derived from peripheral and portal blood, and from patients with IBD stimulated MAIT cells in MR1-dependent manner. CONCLUSION Our findings reveal previously unrecognised roles of liver cells in Ag metabolism and activation of MAIT cells, repression of which creates an opportunity to design antifibrotic therapies. The presence of MAIT cell stimulatory Ags in serum rationalises the observed activated MAIT cell phenotype in liver. Increased serum levels of gut-derived MAIT cell stimulatory ligands in patients with impaired intestinal barrier function indicate that intrahepatic Ag-presentation may represent an important step in the development of liver disease