Loop antenna dosimetry for long time exposure at GSM and UMTS frequencies

(Poster

Modulatory role of 1,25 dihydroxyvitamin D(3) on pancreatic islet insulin release via the cyclic AMP pathway in the rat

1. Previous studies have shown that vitamin D(3) deficiency impairs the insulin response to glucose via an alteration of signal transduction pathways, such as Ca(2+) handling and the phosphoinositide pathway. In the present study the adenylyl cyclase pathway was examined in islets from 3 independent groups: normal rats, 4 weeks-vitamin D(3) deficient rats and one week-1,25 dihydroxyvitamin D(3) (1,25(OH)(2)D(3)) treated rats. 2. We found that the very low rate of insulin release observed in vitamin D(3) deficient rats could be restored in vitamin D(3) deficient islets only with high concentrations of dioctanoyl-cyclic AMP (DO-cyclic AMP), whereas 1,25(OH)(2)D(3) improved the sensitivity of the islets to this exogenous cyclic AMP analogue. 3. The beneficial effect of 1,25(OH)(2)D(3) observed with or without DO-cyclic AMP was protein kinase A-dependent, since the addition of N-[2-(p-bromocinnamylamino) ethyl]-5-isoquinolinesulphonamide (H-89), a specific inhibitor of cyclic AMP-dependent protein kinases, decreased the insulin release of treated rats back to the level seen in vitamin D(3) deficient islets. 4. The low rate of insulin release could not be consistently related to an alteration in cyclic AMP content of the islets. Indeed, low insulin response to a barium + theophylline stimulus observed in vitamin D(3) deficient islets was paradoxically associated with a supranormal cyclic AMP content in the islets. 5. This paradoxical increase in cyclic AMP observed in these conditions could not be attributed to a lower total phosphodiesterase (PDE) activity, although the portion of Ca(2+)-calmodulin-independent PDE was predominant in islets from vitamin D(3) deficient rats. 6. On the other hand, the higher cyclic AMP content of vitamin D(3) deficient islets could be related to an increase in glucagon-induced cyclic AMP synthesis in relation to the hyperglucagonaemia previously observed in vitamin D(3) deficient rats. Since higher concentrations of exogenous glucagon and higher endogenous cyclic AMP concentrations were required in vitro to restore insulin release to normal values, the cyclic AMP-dependent pathways that usually potentiate insulin secretion appeared to be less efficient in relation to an alteration in the post cyclic AMP effector system. 7. 1,25(OH)(2)D(3) exerted a stimulating effect on insulin release via protein kinase A activation but reduced the supranormal cyclic AMP synthesis, thus exerting a differential modulatory influence on biochemical disturbances in islets induced by vitamin D(3) deficiency

Technique non invasive de mise en évidence de micro mouvements tissulaires rythmiques chez l'homme.

International audienc

Technique non invasive de mise en évidence de micro mouvements tissulaires rythmiques chez l'homme.

International audienc

Effect of GSM-900 and -1800 signals on the skin of hairless rats. I: 2-hour acute exposures

International audiencePurpose: The acute influence on the skin of non-ionizing electromagnetic fields in the radiofrequency (RF) range used in mobile telephony has not been widely studied to date. The purpose of this work was to determine whether the cells of hairless rat skin are affected by acute local exposure to Global System for Mobile Communication: GSM-900 or -1800 RadioFrequency Radiation (RFR). Materials and methods: Hairless female rats were exposed or sham-exposed for 2 h to GSM-900 or -1800 signals, using a loop-antenna located on the right part of the rats' back. The local Specific Absorption rate (SAR) at skin level was ca. 5W/kg (5.8±0.4 and 4.8±0.4 W/kg at 900 and 1800 MHz, respectively). A skin biopsy was done at the end of the experiment not only at the location of exposure, but also on the symmetrical part of the back. Results: Analysis of skin sections using Hematoxylin Eosin Saffron (HES) coloration showed no difference in skin thickness or apparent cell toxicity (with no sign of cellular necrosis) among the animal groups. Histological analysis of the epidermis showed that the ratio between cells expressing the antigen Ki-67 (cellular proliferation marker) and the total number of cells remained within the range of normal proliferation ratio for the exposed side of the animal. No Ki-67 labelling was observed at the dermis level. Results on filaggrin, collagen and elastin levels also showed an insignificant influence of RFR. Conclusions: These results do not demonstrate any major physical and histological variations at skin level induced by RFR used in mobile telephony

Effect of GSM-900 and -1800 signals on the skin of hairless rats. II: 12-week chronic exposures

International audiencePurpose: The purpose of this work was to determine whether the cellular components of Hairless-rat skin are affected by a chronic local exposure to non-ionizing radiations of Global Mobile Phone System: GSM-900 or -1800 radiations at specific absorption rate (SAR) 2.5 and 5 W/kg. Materials and methods: A selected part of the right back of five-week old female hairless rats was exposed or sham exposed (n=8) for 2 h per day, 5 days a week, for 12 weeks to GSM-900 or -1800 signals using a loop-antenna. At the end of the experiment, skin biopsies were taken. Results: Analyses of skin sections using hematoxylin eosin saffron (HES) coloration showed no significant difference in skin thickness among the groups. Immunohistochemical analysis of basal lamella cells in radiofrequency radiation (RFR)- exposed epidermis showed that the ratio of the antigen Ki-67 (cellular proliferation marker) positive cells to total lamella cells remained within the range of the normal proliferation ratio. No significant differences in the level of filaggrin, collagen, and elastin were observed among the different groups. Conclusions: The results of this 12-week chronic study do not demonstrate major histological variations in the skin of hairless rats exposed to RFR used in mobile telephony (GSM-900 or -1800)

Effects of mobile telephony signals exposure on radical stress in the rat brain

(Poster

Exposure to Radiofrequency Fields and Heat Shock Protein (Hsp) Expression in the Rat Brain

The expression of heat-shock proteins (HSP) had been observed after exposure to low-level radiofrequency fields (RFR) exposure in worms and in human endothelial cells . These data have been hypothetically linked at best to stress, and at worse to cancer. Further studies failed to confirm these RFR bioeffects, while very few experiments have looked at the expression of Hsp in mammals exposed to RFR. Earlier however, changes in hsp70 mRNA were reported in the brain on rats exposed to a GSM-900 signal. In this study, we have investigated the effects of a single exposure or repeated exposures to two mobile phone-related RFR signals (GSM-1800 MHz and UMTS) on Hsp25 and Hsp70 expression in rat brains. Groups of 8 male Wistar rats were exposed to RFR using a loop antenna at a brain averaged specific absorption rate (BASAR) of 2.6 W/kg. BASAR characterisation was performed as previously described at 900 MHz . Rats were submitted to either a single 2-hour exposure or repeated exposures (two hours/day, five days/week, four weeks). Controls for restraining stress, cage-control and positive-control rats were included. Rats were trained to the setup to avoid stress. At the end of exposure, rat brains were fixed, frozen, and coded. 10 μm sections were prepared and stained with anti-Hsp25 and anti-inducible Hsp70 antibodies. The cerebral cortex and the hippocampus were analysed. The significance of differences between groups was evaluated using the Kruskal-Wallis test. Repeated exposures to UMTS induced an increased expression of Hsp25 and Hsp70 in the retrosplenial cortex and in the hippocampus. A drop in the amount of both Hsp was observed in both the cortex and the hippocampus after a single exposure to GSM-1800, while repeated exposures to GSM-1800 increased Hsp25 expression in the motor and retrosplenial cortex and Hsp70 in the motor cortex. Decreased expression of Hsp, as observed after single exposure to GSM-1800, has been described after treatments with Benzo[a]pyrene or TNFα, but its physiological significance is not clearly established. Our results suggested that repeated exposures to UMTS and GSM-1800 are capable of increasing HSP expression. According to the experimental evidence of the carcinogenic potential of low-level RFR, increase in HSP expression is unlikely to be linked to cancer. We hypothesised that repeated exposures to mobile phone signals may be perceived as a stress and may participate in an adaptative process in the rat brain