Wi-Fi (2.4 GHz) affects anti-oxidant capacity, DNA repair genes expression and, apoptosis in pregnant mouse placenta.

OBJECTIVES: The placenta provides nutrients and oxygen to embryo and removes waste products from embryo's blood. As far as we know, the effects of exposure to Wi-Fi (2.4 GHz) signals on placenta have not been evaluated. Hence, we examined the effect of prenatal exposure to Wi-Fi signals on anti-oxidant capacity, expressions of CDKNA1, and GADD45a as well as apoptosis in placenta and pregnancy outcome. MATERIALS AND METHODS: Pregnant mice were exposed to Wi-Fi signal (2.4 GHz) for 2 and 4 hr. Placenta tissues were examined to measure the MDA and SOD levels. To measure SOD, CDKNA1, GADD45a, Bax, and Bcl-2 expressions were compared by real-time PCR analysis. TUNEL assay was used to assess apoptosis in placenta tissues. The results were analyzed by one-way analysis of variance (ANOVA) using Prism version 6.0 software. RESULTS: MDA and SOD levels had significantly increased in exposed Wi-Fi signal groups (P-value< 0.05). Also, quantitative PCR experiment showed that SOD mRNA expression significantly increased in Wi-Fi signal groups. The data showed that CDKN1A and GADD45a genes were increased in Wi-Fi groups (P-value<0.05). The quantitative PCR and the TUNEL assay showed that apoptosis increased in Wi-Fi groups (P-value<0.05). CONCLUSION: Our results provide evidence that Wi-Fi signals increase lipid peroxidation, SOD activity (oxidative stres), apoptosis and CDKN1A and GADD45a overexpression in mice placenta tissue. However, further experimental studies are warranted to investigate other genes and aspects of pregnancy to determine the role of Wi-Fi radiation on fertility and pregnancy.

The application of ultrasound energy to increase lipid extraction throughput of solid matrix samples (flaxseed).

Ultrasound may reduce lipid extraction times and increase analysis throughput of food materials. Ground flaxseed (25mg aliquots) were extracted in quadruplicate in 2:1 (v:v) chloroform:methanol, 3:2 hexane:isopropanol, 1:1 diethyl:petroleum ether or hexane with exposure to sonication at low frequencies of 20kHz with a 600W ultrasonic processor. Power was automatically varied to maintain constant amplitudes of 20%, 60% and 100% of 240microm for sonication exposures for 5, 10 and 20min, respectively. Total lipid dry weights and quantitative and qualitative fatty acids were determined. Results were compared to a standard 24-h, Folch-based, 2:1 chloroform:methanol extraction. Longer time exposures and higher sonication amplitudes were associated with increases in lipid recoveries. In particular, ultrasound-assisted extraction in 3:2 hexane:isopropanol for only 10min resulted in lipid and fatty acid recoveries similar to the 24-h standard method. Comprehensive testing on a variety of sample matrices and food products is required, but lipid extraction by ultrasound has potential to reduce sample processing time.

Fibrinogen as a risk factor for premature myocardial infarction in Iranian patients: a case control study.

BACKGROUND: Premature myocardial infarction with life-threatening complications may become epidemic in some Asian and African countries and especially Iran. Fibrinogen is considered as one of the probable risk factors of myocardial infarction. The aim of our study was to assess fibrinogen levels as an etiology of premature myocardial infarction in young Iranian men. FINDINGS: A case-control study was conducted between May 2005 and May 2007 to investigate the association between serum total fibrinogen level and myocardial infarction in men aged younger than 55 years admitted to the cardiac care units of Peymanieh and Motahari Hospitals affiliated to Jahrom University of Medical Sciences, Iran. The mean age of patients was 45.2 +/- 4 years in patients with premature myocardial infarction and 47.06 +/- 4.5 years in the control group (p = 0.085). There were no statistically significant relationships between the two groups in history of premature myocardial infarction in their first-degree relatives (p = 0.05), cigarette smoking (p = 0.46), diabetes (p = 0.49), or hypertension (p = 1). The mean plasma fibrinogen in patients (354.9 +/- 60 mg/dL) was elevated markedly compared with the control group (329 +/- 73 mg/dL). Hyperfibrinogenemia (>340 mg/dL) was detected in 81.8% of patients and 57.5% of controls (95% confidence interval, odds ratio = 3.3; p = 0.036). CONCLUSION: This study introduced fibrinogen as a risk factor for premature coronary artery disease in Iranian men.

Induction of antitumor immunity through xenoplacental immunization.

Historically cancer vaccines have yielded suboptimal clinical results. We have developed a novel strategy for eliciting antitumor immunity based upon homology between neoplastic tissue and the developing placenta. Placenta formation shares several key processes with neoplasia, namely: angiogenesis, activation of matrix metalloproteases, and active suppression of immune function. Immune responses against xenoantigens are well known to break self-tolerance. Utilizing xenogeneic placental protein extracts as a vaccine, we have successfully induced anti-tumor immunity against B16 melanoma in C57/BL6 mice, whereas control xenogeneic extracts and B16 tumor extracts where ineffective, or actually promoted tumor growth, respectively. Furthermore, dendritic cells were able to prime tumor immunity when pulsed with the placental xenoantigens. While vaccination-induced tumor regression was abolished in mice depleted of CD4 T cells, both CD4 and CD8 cells were needed to adoptively transfer immunity to naïve mice. Supporting the role of CD8 cells in controlling tumor growth are findings that only freshly isolated CD8 cells from immunized mice were capable of inducing tumor cell caspases-3 activation ex vivo. These data suggest feasibility of using xenogeneic placental preparations as a multivalent vaccine potently targeting not just tumor antigens, but processes that are essential for tumor maintenance of malignant potential.

A novel method of modifying immune responses by vaccination with lipiodol-siRNA mixtures.

The dendritic cell (DC) possesses the ability to stimulate both T helper 1 (Th1) and Th2 responses depending on activation stimuli. Although it is known that chemically or genetically modified DC can be used therapeutically to steer immune responses towards either Th1 or Th2, cellular therapy with ex vivo manipulated DC is clinically difficult. Here we demonstrate a novel method of switching immune responses from Th1 to Th2 through in vivo immune modulation by administration of siRNA. We demonstrate that siRNA targeting of the IL-12p35 gene leads to a Th2 bias in vitro through an IL-10 dependent mechanism. In vivo administration of siRNA admixed with the oil-based contrast agent lipiodol in the presence of antigen and adjuvant induced a deviation in recall response to reduced production of IFN-gamma and augmented IL-4 response using either KLH or ovalbumin. This simple method of in vivo modification of immune response possesses therapeutic potential in Th1-mediated diseases such as multiple sclerosis and autoimmune diabetes.