[Prevalence of nucleotide alterations of EGFR gene in patients with esophageal squamous cell carcinoma in Kerman]

Esophageal Cancer is the sixth fatal cancer in the world. Squamous and adenocarcinoma account for 95% of esophageal cancer. The expression of EGFR has a role in the pathophysiology of epidermal-based malignancies such as esophageal cancer. EGFR is also an important criterion in the evaluation of disease staging and prognosis. The aim of this study was to survey the prevalence of EGFR gene mutations in patients with esophageal cancer by MLPA Technique. A total of 60 parafinated blocks from patients with esophageal cancer were investigated for the presence of EGFR mutations by MLPA technique. EGFR mutation was discovered in 82 percent of samples of which 52% were deletion mostly seen in exon 2 [52%] and duplication mostly seen in exon 27 [54%]. In some cases deletion and/or duplication were seen in more than one exon simultaneously. With regard to the obtained results and since the definitive diagnosis of esophageal cancer is made by biopsy and pathology techniques, it is suggested that all biopsy specimens be detected for EGFR mutations, particularly on exons 2 and 27 in order to achieve a noninvasive molecular diagnostic technique in future

[In vitro evaluation of the enamel surface hardness reduction in primary and permanent teeth caused by two most common acidic soft drinks]

Statement of Problem: Dental erosion is defined as the loss of tooth substance by chemical processes not involving bacteria. Dental erosion has been found to be a common cause of tooth wear. Clinically apparent erosion has been found to be related to dietary factors such as the acid content of the beverages

Purpose: Evaluation of enamel erosion in the primary and permanent teeth as the result of two most common acidic drinks produced in Iranian factories, Mirinda and Pepsi

Materials and Method: The outermost surfaces of 20 primary and 20 permanent teeth were polished flat by using the finest grade sandpaper and water in order to facilitate the proper measurement. The specimens were then prepared by cutting 3-4 mm of the buccal surface of teeth by diamond burs. The specimens were then rinsed with distilled water and stored in 100?10 humidity before testing. The surface micro-hardness of each specimen was measured by micro vickers Hardness tester before, after 5 minutes, and 10 minutes exposure to fresh solution of each drink [10 teeth per test group]. Mann-Whitney and Wilcoxon signed rank tests were used for the estatistical analysis

Results: The results showed that both drinks, Mirinda and Pepsi, produced significant surface hardness loss at 5 and 10 minutes of exposure time [p =0.05]. The amount of erosive effect was changed as the exposure time increased [change from 5 to 10 minutes]. There was no statistically significant difference between the amounts of surface hardness loss in the primary and permanent enamel [p >0.05]

Conclusion: Both drinks may have almost similar but significant erosive effect on the primary and permanent enamel surfaces. Although there wasn't any difference between erosive effect of the two beverages, this effect was increased with increase in time. The primary teeth enamel was not found to be more susceptibe to acidic beverage-induced erosion than the permanent teeth

[PKC mediates endogenous inhibition of myelin repair in the context of local demyelination induced in mice optic chiasm]

Axon regeneration in adult CNS is limited by the presence of inhibitory proteins associated with myelin. Although blocking PKC activity attenuates the ability of CNS myelin to inhibit neurite outgrowth, the role as well as mechanisms underlying the remyelination inhibition in CNS are still largely unknown. Considering the role of PKC in axonal regeneration and the vulnerability of optic chiasm in multiple sclerosis [MS], we assessed the effect of PKC inhibition on remyelination of lysolecithin induced demyelinated optic chiasm. Demyelination was induced by stereotaxic intra-chiasmatic injection of 1 micro l lysolecithin [%1] in male mice. Intracerebroventricular daily injection of a PKC inhibitor [GO6976] was done for 14 days post-lesion. Demyelination and remyelination patterns in optic chiasm were confirmed through histological verification and electrophysiological study using Luxol fast blue staining and visual evoked potentials [VEP] recording, respectively. In lysolecithin treated animals, demyelination was mostly marked at days 3 and 7 post-lesion and an incomplete remyelination occurred at day 14 post-lesion. VEP recording showed increased P-latency at the days 3 and 7 post-lesion while it partially decreased at day 14. Following the inhibition of PKC, while the extent of demyelination and P-latency slightly decreased at the days 3 and 7 post-lesion, it recovered at day 14. VEP recording data were confirmed by histological verification. Inhibition of PKC activity could represent a potential therapeutic approach for stimulating the remyelination process in the context of multiple sclerosis