Cytological effects of pulsed electromagnetic fields and static magnetic fields induced by a therapeutic device on in vivo exposed rats

Background: There is a trend towards the use of magnetic fields in medicine. Pulsed electromagnetic fields (PEMFs) technology was based upon 20 years of fundamental studies on the electromechanical properties of bone and other connective tissues. More recently, these magnetic fields have been used to treat several health conditions. There remains continuing concern that exposure to electromagnetic devices may cause adverse effects. The aim of the present study was to investigate the cytological effects induced in rats exposed in a patented medical device that uses PEMFs combined with static magnetic fields (SMFs).Material and Methods: Thirty sexually mature 14-week-old male and female Sprague Dawley rats were distributed into three groups: (a) 5 males and 5 females (independently) exposed to PEMFs combined with SMFs, (b) animals treated with SMFs only, and (c) non-exposed animals. Acridine orange fluorescent-staining micronucleus test and male germ cells analysis were performed according to standardized techniques.Results: A lack of evidence for alterations on micronucleus frequency, on polychromatic erythrocytes percentage, and on sperm counts and morphological characteristics of male germ cells were found in mature rats exposed to PEMFs medical device compared to non-exposed animals.Conclusions: This study suggests that the applied magnetic field generated in a therapeutic device did not have any detectable cytotoxic or genotoxic effect in exposed rats. In view of these findings and the contradictory reports in the literature, it is necessary to carry out more research to help clarify the controversy concerning cytogenotoxic risk associated with therapeutic magnetic fields exposures.Keywords: Cytotoxicity, pulsed electromagnetic fields, static magnetic fields, micronuclei, sperm abnormalitie

Infection and coinfection by human papillomavirus, Epstein–Barr virus and Merkel cell polyomavirus in patients with squamous cell carcinoma of the larynx: a retrospective study

Background Human papillomavirus (HPV) is recognized as an important risk factor for laryngeal carcinogenesis. Although HPV-16 and 18 have been strongly implicated, the presence of other high-risk HPV (HR-HPV) genotypes or the coinfection with Epstein-Barr virus (EBV) or Merkel cell polyomavirus (MCPV) may increase the risk, but their etiological association has not been definitively established. Methods We characterized the genotype-specific HPV and the frequency of EBV and MCPV infections through the detection of their DNA in 195 laryngeal specimens of squamous cell carcinoma (SCC) histologically confirmed. Results HPV DNA was detected in 93 (47.7%) specimens. HPV-11 was the most frequent with 68 cases (73.1%), and HPV-52 was the most frequently HR-HPV found with 51 cases, which corresponds to 54.8% of all HPV-positive specimens. EBV DNA was detected in 54 (27.7%) tumor tissue specimens of which 25 (46.3%) were in coinfection with HPV. MCPV DNA was detected only in 11 (5.6%) cases of which 5 (45.4%) were in coinfection with an HR-HPV. No association between the presence of DNA of the three examined viruses and the patient smoking habits, alcohol consumption, age, the keratinization status, differentiation grade, or localization of the tumor in the larynx were found. Discussion HPV-52 was the most prevalent HR-HPV, which may suggest that this and other genotypes in addition to HPV-16 and 18 could be considered for prophylaxis. However, further studies including non-cancer larynx cases and the evaluation of other molecular markers and viral co-infection mechanisms are needed to determine the role of the different HR-HPV genotypes, EBV, and MCPV in the etiology of SCC of the larynx

Leptin receptor expression during the progression of endometrial carcinoma is correlated with estrogen and progesterone receptors

Introduction : The hormone leptin, which is produced in the adipose tissue, may influence tumorigenesis directly via its receptor (Ob-R). Thus, a role for Ob-R in endometrial carcinogenesis has been proposed. However, most studies neither included samples of the entire histological progression of endometrial carcinoma nor examined Ob-R jointly with the estrogen and progesterone receptors (ER and PR, respectively). Material and methods: To determine the fluctuations of Ob-R, ER, and PR during the histological progression of endometrial carcinoma, we assessed their expression via immunohistochemistry (IHC) in six histological types of endometrium (proliferative, secretory, nonatypical and atypical hyperplasia, and endometrioid and nonendometrioid endometrial carcinoma), in which we performed histopathological and digital scoring for the quantification of receptors. Results: We found that Ob-R expression was positively correlated with that of ER and PR (r = 1, p < 0.001; r = 0.943, p < 0.005, respectively), and there was a significant difference in Ob-R expression among proliferative normal endometrium, hyperplasias, and carcinomas, according to their relative digitally scored Ob-R expression (p < 0.001). In addition, we observed that Ob-R expression in the secretory endometrium was more similar to that of carcinomas than to its proliferative counterpart. Conclusions : These results indicate that Ob-R expression fluctuates during endometrial carcinogenesis in correlation with ER and PR, suggesting that Ob-R expression in vivo is highly dependent on estrogen and progesterone activities in the endometrium and on its ER and PR status, as suggested previously by in vitro studies