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New observations of the eclipsing binary system V1848 Ori were carried out using the V filter resulting in a determination of new times of minima and new ephemeris were obtained. We presented the first complete analysis of the system’s orbital period behavior and analysis of O-C diagram done by the GA and MCMC approaches in OCFit code. The O-C diagram demonstrates a sinusoidal trend in the data; this trend suggests a cyclic change caused by the LITE effect with a period of 10.57 years and an amplitude of 7.182 minutes. It appears that there is a third body with mass function of f (m3) = 0.0058 M⊙ in this binary system. The light curves were analyzed using the Wilson-Devinney code to determine some geometrical and physical parameters of the system. These results show that V1848 Ori is a contact W UMa binary system with the mass ratio of q = 0.76 and a weak fillout factor of 5.8%. The O’Connell effect was not seen in the light curve and there is no need to add spot.

In the field of determination of vitamin B9 (folic acid, FA), we have described the development of a sensitive electrochemical sensor through promoting the screen-printed electrode (SPE) and taking the advantage of zinc ferrite magnetic nanoparticles (ZnFe2O4MNPs). Cyclic voltammetry (CV) experiments demonstrated the powerful activity of ZnFe2O4MNPs/SPE for electrooxidation of FA by showing the prominent oxidation peak at 600 mV vs. Ag/AgCl. By differential pulse voltammetry (DPV) measurements, a linear relation between current response and concentration of vitamin B9 was determined in the range of 1.0–100.0 µM, and detection limit is found to be 0.3 µM (S/N=3). Except high sensitivity, the developed sensor demonstrated high stability, reproducibility and repeatability, and was also successfully applied to specify FA in real samples of vitamin B9 tablets and human urine.

Abstract Background Squamous cell carcinoma of esophagus (SCCE) occurs at a high incidence rate in certain parts of the world. This feature necessitates that different aspects of the disease and in particular genetic characteristics be investigated in such regions. In addition, such investigations might lead to achievement of molecular markers helpful for early detection, successful treatment and follow up of the disease. Adenomatous Polyposis Coli (APC) promoter hypermethylation has been shown to be a suitable marker for both serum and solid tumors of adenocarcinoma of esophagus. We investigated the status of APC promoter hypermethylation in Iranian patients, compared the results with the former studies, and evaluated its applicability as a candidate molecular marker by examining association between survival of SCCE patients and APC promoter methylation. Methods For evaluating the status of APC promoter hypermethylation and its association with SCCE, a qualitative methylation specific PCR (MSP) was used. DNA was extracted and digested with an appropriate restriction enzyme, treated with sodium bisulfite in agarose beads and amplified in two-step PCR reaction by applying either methylated or unmethylated promoter specific primers. Universally methylated DNA and methylase treated blood DNA of healthy donors were used as positive controls as well. Survival of patients was followed up for two years after treatment and survival rate of patients with methylated APC promoter was compared with that of unmethylated patients. Results Assessment of APC promoter methylation revealed that normal tissues were unmethylated, while twenty out of forty five (44.4%) tumor tissues were hypermethylated either in one or both alleles of APC. Among the tissues in which methylation was detected, seven were hypermethylated in both alleles while the other thirteen were hypermethylated in one of the two alleles of APC. Analyzing two-year survival rate of patients with respect to promoter hypermethylation showed a lower rate of survival for patients with methylated APC promoter following their treatment. Further investigation into the association between promoter hypermethylation and tumor differentiation status indicated that patients with well differentiated tumors were more likely to develop promoter hypermethylation. Conclusion Observing similar level of APC promoter hypermethylation in patients with SCCE in this high risk region and comparing it with other parts of the world could support the hypothesis that a common molecular mechanism might be involved in tumorigenesis of SCCE. In addition, the higher rate of two-year survival for patients with unmethylated APC promoter as well as its relationship with tumor differentiation would suggest that this tumor suppressor could be an appropriate candidate molecular marker for evaluating tumor malignancy and predicting survival of patients subsequent to treatment.