No effect of mobile phone-like RF exposure on patients with atopic dermatitis.

This study investigates the effect of exposure to a mobile phone-like radiofrequency (RF) electromagnetic field on people with atopic dermatitis (AD). Fifteen subjects with AD were recruited and matched with 15 controls without AD. The subjects were exposed for 30 min to an RF field at 1 W/kg via an indoor base station antenna attached to a 900 MHz GSM mobile phone. Blood samples for ELISA analysis of the concentration of substance P (SP), tumor necrosis factor receptor 1 (TNF R1), and brain derived neurotrophic factor (BDNF) in serum were drawn before and after the provocation (exposure/sham). Baseline heart rate and heart rate variability, local blood flow, and electrodermal activity were also recorded. No significant differences between the subject groups were found for baseline neurophysiological data. The cases displayed a serum concentration of TNF R1 significantly higher than the control subjects and a significantly lower serum concentration of BDNF in the baseline condition. For SP there was no difference between groups. However, no effects related to RF exposure condition were encountered for any of the measured substances. As to symptoms, a possible correlation with exposure could not be evaluated, due to too few symptom reports. The result of the study does not support the hypothesis of an effect of mobile phone-like RF exposure on serum levels of SP, TNF R1, and BDNF in persons with AD.

Apoptosis induced by low-dose and low-dose-rate radiation.

BACKGROUND: It has been claimed that external radiation, as a treatment modality for malignant diseases, partly induces apoptosis. It is not known, however, whether therapeutic low-dose and low-dose-rate radiation are able to induce apoptosis. METHODS: The effect of low-dose radiation on apoptosis induction in HeLa Hep2 cells was studied, and quantitation of the apoptotic cells was performed by immunocytochemistry using TdT-mediated dUtp-x Nick End Labeling (TUNEL) technology and the M30 CytoDEATH antibody method. RESULTS: When TUNEL staining was used to quantify apoptosis in untreated HeLa Hep2 cells kept in culture, approximately 5 plus minus 3% of the cells showed positive staining without any treatment. In the first experiment, the HeLa Hep2 cells were exposed to gamma radiation (i.e., 0.5, 1, 2, 5, 10, and 15 grays [Gy]) from a cobalt-60 radiation source delivering a dose rate of 0.80 Gy/min. The radiated cells were cultivated for 5, 10, 24, 48, 72 and 168 hours after irradiation. Radiation doses below 2 Gy did not cause any significant apoptosis, but between 5 and 15 Gy significant apoptosis was observed, with peak values at 5 Gy (P < 0.001). Up to 60% of the investigated cells were shown to display apoptosis. Time to this peak value was 168 hours after irradiation. The HeLa Hep2 cells were exposed to doses of 2, 5, and 10 Gy at a 10-fold lower dose rate (0.072 Gy/min). The cells that achieved a dose below 2 Gy did not present increased apoptosis. At doses above 2 Gy, however, the cells again demonstrated significant apoptosis. Up to 24 hours following irradiation, no apoptosis could be documented, whereas beyond 24 and up to 168 hours a highly significant apoptosis induction was observed. Significant cytotoxicity was confirmed by chromium-51 release from the cells at 5 Gy. CONCLUSIONS: Low-dose and low-dose-rate radiation are able to induce significant apoptosis, and apoptosis may be one of the mechanisms by which low-dose radiation causes growth inhibition.

Idiotypic-anti-idiotypic complexes and their in vivo metabolism.

BACKGROUND: Different strategies can be used to improve the tumor:non-tumor ratio of radiolabeled antibodies in immunotargeting. One approach is to use secondary antibodies to clear out redundant, circulating primary antibodies. In the current study, the in vitro complex formation and in vivo clearing capabilities and metabolism of the monoclonal antibody TS1 and its monoclonal anti-idiotype, alphaTS1, were studied. METHODS: Complex formation studies were performed using polyacrylamide gel electrophoresis (PAGE), gel permeation chromatography, and electron microscopy. The clearance and metabolism of the complexes were studied in nude mice. RESULTS: PAGE and gel permeation chromatography showed that more than 70% of the antibodies formed complexes. The electron microscopy studies revealed that the complexes formed between TS1 and alphaTS1 are mainly ring-shaped (66.6-73.4%), comprising 4 to > 8 antibodies. These rings consist of equal numbers of idiotype and anti-idiotype. The most commonly observed complexes were tetrameric rings (26.8-40.5%), hexameric rings (10.7-11.9%), and rings containing more than eight monoclonal antibodies (6.6-14-4%). The in vivo study illustrated that within 24 hours 80% of the total nuclide content had been degraded and excreted via the urine, compared with 25% for similarly treated mice that did not receive any anti-idiotype. CONCLUSIONS: Interestingly, the electron microscopy study demonstrated that dimers were rare (0.4-1.2%), probably reflecting a location of epitopes incompatible with tight, sterically constrained dimeric interactions; insufficient flexibility of the immunoglobulin G1 subtype hinge regions; or both. The anti-idiotypic clearing mechanisms proved efficient in nude mice. In vivo metabolic studies indicate that the accumulation and degradation of TS1/alphaTS1 immune complexes, to a large extent, take place in the liver, where a substantial amount was detected as soon as 1 hour after anti-idiotype injection.

The combination of external beam radiotherapy and experimental radioimmunotargeting with a monoclonal anticytokeratin antibody.

BACKGROUND: Doses to tumors of up to 80 grays (Gy) have been postulated to eradicate solid experimental tumors with radiommunotargeting, but this value has proved difficult to reach. Combining two treatment modalities, external beam radiotherapy and radioimmunotargeting, could potentially give rise to a number of advantages. METHODS: The purpose of this study was to detect potential benefits with different treatment timing strategies when combining external beam radiotherapy and radioimmunotargeting, with the anticytokeratin monoclonal antibody (MAb) TS1 injected into a nude mouse model carrying subcutaneous human HeLa Hep 2-cell tumors. Cytokeratins are present in necrotic regions within tumors, thereby providing a potential increase in binding sites for TS1 if combined with external beam radiotherapy. External beam radiotherapy was given before, after, and simultaneously with injection of radiolabeled MAb. RESULTS: The highest yields in terms of total accumulated dose (Gy), percentage of injected activity per gram of tumor tissue, and accumulated dose per injected activity (Gy/MBq) were seen in the group receiving external beam radiotherapy prior to MAb-injection. CONCLUSIONS: Enhanced effects may be achievable by combining external beam radiotherapy with experimental radioimmunotargeting using the monoclonal anticytokeratin antibody TS1, if the radiotherapy is given prior to MAb injection.