There are few researches in literature that mention the use of the apex locator in deciduous teeth and working length is obtained through radiographies. Objective: The purpose of this research was to compare the radiographic and the electronic method to obtain the working length in deciduous molars. Material andmethods: Twelve molar teeth were used. The specimens in the visual method had their root length measured through the passive insertion of a 10 K-file with a silicone stop within root canal until its tip was seen at the apical foramen. The working length was measured through radiographs or using the apex locator Root ZX II. The mean between the examiners was submitted to the variance analysis (ANOVA). Results: Statistically significant differences were found between the visual method and the radiographic method (p < 0.001). There was no significant difference between the working length measurements in visual method and those obtained with the apex locator (p = 0.1319). Conclusion: The apex locator is indicated as a clinical implementation for endodontic treatment in primary teeth.
Palmitoleic acid (16:1n7) enhances whole body glucose disposal, suppresses hepatic steatosis and modulates triacylglycerol (TAG) metabolism in adipocytes. Here, we investigated the effects of 16:1n7 on glucose uptake and TAG synthesis by primary adipocytes. METHODS: Primary epididimal adipocytes from C57BL6 mice treated with 16:1n7 (300 mg/kg/day), oleic acid (18:1n9, 300 mg/kg/day) or water by gavage for 10 days were evaluated for 2‐deoxy‐D‐[3H]‐glucose uptake on basal and insulin‐stimulated (10 nmol/liter) conditions, phosphorylated and total AKT content, 14C‐glucose incorporation into fatty acids or glycerol and 14C‐acetate incorporation into fatty acids. RESULTS: Treatment with 16:1n7 or 18:1n9 did not affect body weight, food intake, masses of white adipose depots and plasma levels of free fatty acids, insulin and glucose. Treatment with 16:1n7 increased basal (~3 fold) and insulin‐stimulated (~2 fold, p<0.05) glucose uptake on epididimal adipocytes compared with water and 18:1n9 treatment. There were no changes on acetate or glucose incorporation into fatty acids among treatments, but the 16:1n7 increased glucose incorporation in glycerol‐TAG (H2O=227.2±9.1; 18:1n9=226.6±24.6; 16:1n7=307.2±19 nmol/106 cells, p<0.05). The treatments did not change the phosphorylated and total AKT content. CONCLUSION: 16:1n7 raised basal and insulin‐stimulated glucose uptake without affecting AKT. Furthermore, 16:1n7 increased the generation of glycerol‐3‐phosphate from glucose on epididimal adipocytes without affecting fatty acid synthesis from this hexose. Grant Funding Source: Supported by FAPESP
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