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In the present research, an ultrasound-assisted magnetic solid-phase extraction coupled with a gas chromatography-mass spectrometry hybrid system was developed for the extraction/determination of trace amounts of polycyclic aromatic hydrocarbons in high-consumption soft drinks and non-alcoholic beers in Iran using magnetite graphene oxide adsorbent. The magnetite graphene oxide was characterized by scanning electron microscope, transmission electron microscopy, Fourier-transform infrared spectroscopy, X-ray diffraction, and vibrating-sample magnetometer techniques. The highest extraction recovery (73.05%-95.56%) and enrichment factor (90.65-106.38) were obtained at adsorbent mass: 10 mg, adsorption time: 30 min, salt addition: sodium chloride 10% w/v, desorption time: 20 min, eluent type: hexane: acetone (1:1, v/v), and desorption solvent volumes: 200 μl. Under optimum conditions, the linearity range for polycyclic aromatic hydrocarbons determination was 0.2-200 ng/ml with a coefficient of determination 0.993, the limit of detection = 0.09-0.21 ng/ml, the limit of quantitation = 0.3-0.7 ng/ml, and relative standard deviation 8.1%, respectively. Relative recoveries in spiked real samples ranged from 94.67 to 109.45% with a standard deviation 6.05%. The proposed method is effective, sensitive, and reusable and it is promising for the analysis of polycyclic aromatic hydrocarbons residues in environmental samples.

In the present study, the magnetic NH

Background Breast cancer is a type of cancer with a high incidence and mortality rate worldwide. Change in epigenetic mechanisms enhances cancer cell progression. Histon deacetylase 2 (HDAC2) was found to act as a potential oncogene in different malignancies. For better understanding the mechanisms related to breast cancer development, we investigated the role of HDAC2 in breast cancer and the inhibitory effect of miR-646 on this oncogene. Methods A total of thirty cancerous tissues and 30 adjacent non-cancerous specimens and also three breast cancer cell lines were enrolled in the study. Quantitative reverse transcriptase PCR (qRT-PCR) was employed to detect the HDAC2 and miR-646 expression level in the studied samples. The biological roles of HDAC2 and miR-646 were investigated through manipulating the expression level of HDAC2 or miR-646 in breast cancer cells. Finally, we evaluated whether the HDAC2 is a direct target for miR-646. Results In this study, we found HDAC2 is significantly upregulated in cancerous specimens and cell lines compared to non-cancerous tissues and normal cell line. On the other hand, miR-646 expression was decreased in clinical specimens and breast cancer cells compared to non-cancerous samples. Knocking out of the HDAC2 and overexpression of miR-646 inhibited breast cancer cell growth but promoted cell death, while untreated groups showed inverse results. Furthermore, we showed that in the breast cancer cells, miR-646 regulates the progression and proliferation by suppressing HDAC2. Conclusion Taken together, our study identified a miR-646/HDAC2 regulatory function in the breast cancer development and introduced a therapeutically target for breast cancer.

Background:: Although opium is frequently used for the synthesis of applied medications, its deleterious effects on vital organs and biomarkers have been reported. Objectives:: The present study came to address the degree of liver inflammation following inhaled opium use and compare it with the severity of liver inflammation in the animal group receiving cigarette smoking. Materials and Methods:: In this experimental study, 40 Syrian golden hamsters were randomly divided into five groups as group not receiving any regimen as the control, A: group receiving inhaled opium, B: group receiving cigarette smoke, C: group receiving inhaled opium with double dosage of the second group, D: group receiving inhaled opium and cigarette smoke concurrently. The degree of inflammation was evaluated by various scoring systems including Knodell/original HAI score, Ishak/modified HAI score, METAVIR score and two other ordinal inflammatory scoring approaches. Results:: Histological interpretation of the liver samples showed similar mean Knodell/original HAI score, Ishak/modified HAI score, and METAVIR score across the five groups. According to other two ordinal methods for scoring inflammation, there were also no significant differences in the degree of inflammation activity across the interventional groups and the control. Conclusions:: The inflammatory response to cigarette smoking seems to be similar to the use of inhaled opium; however, similarity of the inflammation degree between inhaled opium users and control experiments should be taken into consideration.

The role of aquaporin-4 (AQP4) and interleukin-6 (IL-6) in the development of brain edema post-traumatic brain injury (TBI) has been indicated. The present study was designed to investigate the effect(s) of administration of progesterone (P) and/or estrogen (E) on brain water content, AQP4 expression, and IL-6 levels post-TBI. The ovariectomized rats were divided into 11 groups: sham, one vehicle, two vehicles, E1, E2, P1, P2, E1 + P1, E1 + P2, E2 + P1, and E2 + P2. The brain AQP4 expression, IL-6 levels, and water content were evaluated 24 h after TBI induced by Marmarou’s method. The low (E1 and P1) and high (E2 and P2) doses of estrogen and progesterone were administered 30 min post-TBI. The results showed that brain water content and AQP4 expression decreased in the E1, E2, P1, and P2-treated groups. The administration of E1 decreased IL-6 levels. Addition of progesterone decreased the inhibitory effect of E1 and E2 on the accumulation of water in the brain. Administration of E1 + P1 and E1 + P2 decreased the inhibitory effect of E1 on the IL-6 levels and AQP4 protein expression. Our findings suggest that estrogen or progesterone by itself has more effective roles in decrease of brain edema than combination of both. Possible mechanism may be mediated by the alteration of AQP4 and IL-6 expression. However, further studies are required to verify the exact mechanism.

Background Serious health problems and socioeconomic consequences of the illicit use of opiates have been proved in both developed and developing societies Objectives We aimed to evaluate" The effects of opiate addiction through different administration routes on pulmonary inflammation and its severity." Materials and Methods Our experiments were performed on eighteen adult male Syrian golden hamsters which were allocated to one of the three groups (n = 6): control group which did not receive opiate; the first study group were administered oral opiate via stomach tube; and another study group were administered inhaled opiate. After four weeks, all hamsters were anesthetized with diethyl ether and their lung tissues were isolated for pathological assessment. Results Severe perivascular inflammation was detected in 33.3% of the samples with oral opiate dependence and 20% of the cases addicted to opiate through inhalation. Also, severe peribronchial inflammation was observed in only 20% of the samples addicted to inhaled opiate and was not found in the other groups. No significant differences were found in the severity of perivascular and peribronchial inflammation across the three groups. Although the mean of total inflammation scale in the subjects with oral opiate dependence (3.00 ± 1.79) was numerically higher than that in the inhaled dependence group (1.40 ± 2.60) and the controls (2.25 ± 1.26), this difference was not statistically significant. Conclusions Administration did not influence the appearance or severity of pulmonary inflammation in animal models addicted to opiate.