Assessment of potential effects of the electromagnetic fields of mobile phones on hearing

BACKGROUND: Mobile phones have become indispensable as communication tools; however, to date there is only a limited knowledge about interaction between electromagnetic fields (EMF) emitted by mobile phones and auditory function. The aim of the study was to assess potential changes in hearing function as a consequence of exposure to low-intensity EMF's produced by mobile phones at frequencies of 900 and 1800 MHz. METHODS: The within-subject study was performed on thirty volunteers (age 18–30 years) with normal hearing to assess possible acute effect of EMF. Participants attended two sessions: genuine and sham exposure of EMF. Hearing threshold levels (HTL) on pure tone audiometry (PTA) and transient evoked otoacoustic emissions (TEOAE's) were recorded before and immediately after 10 min of genuine and/or sham exposure of mobile phone EMF. The administration of genuine or sham exposure was double blind and counterbalanced in order. RESULTS: Statistical analysis revealed no significant differences in the mean HTLs of PTA and mean shifts of TEOAE's before and after genuine and/or sham mobile phone EMF 10 min exposure. The data collected showed that average TEOAE levels (averaged across a frequency range) changed less than 2.5 dB between pre- and post-, genuine and sham exposure. The greatest individual change was 10 dB, with a decrease in level from pre- to post- real exposure. CONCLUSION: It could be concluded that a 10-min close exposure of EMFs emitted from a mobile phone had no immediate after-effect on measurements of HTL of PTA and TEOAEs in young human subjects and no measurable hearing deterioration was detected in our study

Is YouTube an accurate and/or comprehensive source of information for monosymptomatic enuresis nocturna?

[Abstract Not Available

Protective effect of sildenafil on liver injury induced by intestinal ischemia/reperfusion

Background This study evaluated the protective effect of sildenafil on liver injury induced by intestinal ischemia-reperfusion. Methods Forty female Sprague Dawley rats were divided into 4 groups: sham-control (SC), ischemia (I), ischemia-reperfusion (IR), and ischemia-reperfusion + sildenafil (SIL; sildenafil gavaged at 50 mg/kg before operating). A 2-h ischemia-reperfusion was performed by clamping the superior mesenteric artery. Liver function, plasma alanine (ALT) and aspartate (AST) aminotransferase, and intestinal and liver malondialdehyde (MDA) were measured at the end of the experiment. Intestinal and liver tissue damage was examined by histology. Liver samples were immunologically stained for endothelial nitric oxide synthase (eNOS) and proliferating cell nuclear antigen (PCNA). Results The ALT and AST levels were highest in the IR group and were lower in the SIL group (p 0.05). Intestinal damage based on Chiu scoring was more severe in the IR than in the SIL group (p < 0.05). Sildenafil reduced damage and also increased eNOS and PCNA immunoreactivity in liver tissue. Conclusions Sildenafil shows a protective effect on intestinal ischemia-reperfusion-induced liver injury, possibly by decreasing vascular resistance through increased nitric oxide levels. © 2013 Elsevier Inc

Effects of curcumin on apoptosis and oxidoinflammatory regulation in a rat model of acetic acid-induced colitis: The roles of c-Jun N-Terminal Kinase and p38 mitogen-activated protein kinase

The present study evaluated the effects of curcumin on epithelial cell apoptosis, the immunoreactivity of the phospho-c-Jun N-terminal kinase (JNK) and phospho-p38 mitogen-activated protein kinases (MAPKs) in inflamed colon mucosa, and oxidative stress in a rat model of ulcerative colitis induced by acetic acid. Rats were randomly divided into three groups: control, acetic acid, and acetic acid+curcumin. Curcumin (100 mg/kg per day, intragastrically) was administered 10 days before the induction of colitis and was continued for two additional days. Acetic acid-induced colitis caused a significant increase in the macroscopic and microscopic tissue ranking scores as well as an elevation in colonic myeloperoxidase (MPO) activity, malondialdehyde (MDA) levels, and the number of apoptotic epithelial cells in colon tissue compared to controls. In the rat colon, immunoreactivity of phospho-p38 MAPK was increased, whereas the phospho-JNK activity was decreased following the induction of colitis. Curcumin treatment was associated with amelioration of macroscopic and microscopic colitis sores, decreased MPO activity, and decreased MDA levels in acetic acid-induced colitis. Furthermore, oral curcumin supplementation clearly prevented programmed cell death and restored immunreactivity of MAPKs in the colons of colitic rats. The results of this study suggest that oral curcumin treatment decreases colon injury and is associated with decreased inflammatory reactions, lipid peroxidation, apoptotic cell death, and modulating p38- and JNK-MAPK pathways. © Mary Ann Liebert, Inc

Vitamin E modulates apoptosis and c-jun N-terminal kinase activation in ovarian torsion-detorsion injury

The aim of this study was to evaluate the role of vitamin E in follicular degeneration and to assess histopathological and biochemical changes following ischemia-reperfusion (IR) injury in rat ovaries. Twenty-eight Wistar albino rats were randomly divided into four groups: sham, 4. h torsion, 24. h detorsion, and a vitamin E group. Thirty minutes before detorsion, a single dose of 200. mg/kg vitamin E was administered intraperitoneally. The ovarian histology score was determined, serum levels of malondialdehyde (MDA) and myeloperoxidase (MPO) were measured. The apoptosis of granulosa cells and the phospho-c-jun N-terminal kinase (p-JNK) and phospho-p38 (p-p38) immunoreactivities of these cells were determined. MDA and MPO levels were significantly increased in the torsion and detorsion groups. Hemorrhage, edema, and congestion were also apparent in these groups. In addition, the apoptotic index and the immunoreactivity of p-JNK were highest in the detorsion group, which also showed marked follicular degeneration. However, p-p38 activity was not affected by torsion-detorsion (TD) induction. Vitamin E ameliorated TD-induced histological alterations. It also decreased serum levels of MDA and MPO, reduced the activity of p-JNK in the ovaries, and reduced numbers of apoptotic follicular cells. In conclusion, these data indicate that vitamin E attenuated ovarian follicular degeneration by inhibiting the immunoreactivity of p-JNK and reducing the apoptosis of granulosa cells. © 2013 Elsevier Inc.2011-121The authors acknowledge Trakya University Research Center, Edirne, Turkey for the financial support (project no: 2011-121 )