No abstract

Levels of polychlorinated biphenyls (PCBs) and polybrominated diphenyl ethers (PBDEs) were measured in 53 human adipose tissue samples. The samples consisted of adipose tissue from 31 men and 22 women having a mean age of 53 years. No information about diet or occupational exposure was collected. Cleanup was performed using a glass column containing acidified silica, deactivated alumina, and anhydrous sodium sulphate. Subsequently, samples were analyzed by high-resolution gas chromatography/tandem mass spectrometry. PBDE concentrations (sum of BDEs 28, 47, 99, 100, 154, 153, and 183) ranged between 1.23 and 57.2 ng g(-1) lipid weight and were comparable with levels in samples from other European countries. The sum of seven International Council for the Exploration of the Sea (ICES) indicator PCB congeners (PCBs 28, 52, 101, 118, 138, 153, and 180) ranged from 126 to 2090 ng g(-1) lipid weight. No age dependency was found for PBDEs (Pearson correlation -0.023, p = 0.873), whereas PCBs showed higher correlation coefficients with age (Pearson correlation 0.613, p < 0.0005). There was no relationship between PBDE and PCB levels (Pearson correlation -0.010, p = 0.943).

The presented data are the result of a reappraisal of the biocompatibility properties of titanium alloys. An in vitro study has been conducted using Hanks' solution with four different additional compounds (EDTA, l-leucine, Na-citrate, and 8-hydroxyquinoline). A measurable dissolution rate was observed for Ti and Al in a solution containing EDTA and for Ti, Al, and V for a solution containing Na-citrate. The dissolution kinetics are discussed and explained in terms of the composition of the surface layers. The results contain useful introductory information for an extended study of media allowing representative in vitro simulation of the in vivo behavior of titanium alloys.

A 5-day administration of 250 mg of simmondsin/kg of body weight did not have any toxicological influences on liver, pancreas, and kidneys using several biochemical parameters. Anatomopathological investigation of kidney, liver, pancreas, stomach, intestine, testis, and seminal vesicle also did not demonstrate any pathological change. Since the concentrations of CN- and of SCN- in the blood are not elevated, it is concluded that there are no indications for a liberation of HCN during the metabolism of simmondsin in the rat. The food intake inhibition and weight-reducing effect of gastrally intubated simmondsin in rats has been confirmed, but there are no indications that HCN causes the food intake reduction or the weight loss after simmondsin intake in rats

No abstract