1800 MHz radiofrequency (mobile phones, different Global System for Mobile communication modulations) does not affect apoptosis and heat shock protein 70 level in peripheral blood mononuclear cells from young and old donors.

PURPOSE: To study if prolonged in vitro exposure to 1800MHz radiofrequency (RF) could exert an effect on human peripheral blood mononuclear cells (PBMC) from young and elderly donors by affecting apoptosis, mitochondrial membrane potential and heat shock protein (HSP) 70 levels. MATERIALS AND METHODS: Endpoints were analysed in the presence or absence of the apoptosis-inducing agent 2-deoxy-D-ribose. Three different signal modulations typical of the Global System for Mobile communication (GSM) system were applied. The modulations are widely used in mobile telephony (GSM Basic, discontinuous transmission [DTX] and Talk) at specific absorption rates of 1.4 and 2.0 W kg(-1). RESULTS: In all conditions and for all endpoints tested, there was no significant difference between RF- and sham-exposed cells. CONCLUSION: 1800MHz RF could not induce apoptosis by itself or affect the apoptotic phenomenon when induced by an apoptotic agent. Moreover, RF did not modify the mitochondrial functionality and the expression of HSP 70.

Glycine adjuvant therapy to conventional neuroleptic treatment in schizophrenia: an open-label, pilot study.

In an open-label study, glycine was administered orally (10.8 g/day in three divided doses) to six chronically psychotic patients, as an adjunct to conventional neuroleptic therapy, for periods extending from 4 days to 8 weeks. Glycine was administered in an effort to facilitate endogenous glutamatergic transmission at the level of the N-methyl-D-aspartate (NMDA) receptor complex, since a glutamatergic deficiency in the pathophysiology of schizophrenia has been postulated. Therapeutic efficacy was assessed with standardized psychiatric rating scales. Beneficial effects on behavioral symptomatology were observed in two patients, whereas two others worsened. In one of the two responders, clinical deterioration occurred after glycine withdrawal consistent with a positive adjuvant effect in this patient. However, glycine rechallenge in this patient was not associated with the clinical improvement seen during the initial glycine period. Clinical worsening was not observed after glycine discontinuation in the second responder. Glycine administration reduced neuroleptic-induced muscle stiffness and extrapyramidal dysfunction in three of the six patients. All patients tolerated the clinical trial. The limited penetrability of glycine across the blood-brain barrier is a major limitation of this approach to facilitating glutamatergic transmission at the level of the NMDA receptor complex.