An ex vivo evaluation of a new root canal irrigation technique with intracanal aspiration.

AIM: To evaluate the effectiveness of a new root canal irrigation technique with intracanal aspiration in removing the smear layer and to assess irrigant extrusion ex vivo. METHODOLOGY: Thirty-five instrumented canals of extracted human canine teeth that had been resected apically by removing 3 mm of the root tip were divided into one control and four experimental groups of seven teeth each. The roots were fixed in a plastic case and surrounded with normal saline agar coloured with 1% acid red. No irrigation was performed in the control teeth. Each root canal in the experimental groups was irrigated with 9 mL of 14% ethylenediaminetetraacetic acid for 3 min, and then with 6 mL of 6% sodium hypochlorite (NaOCl) for 2 min. In the intracanal aspiration technique, the irrigant was delivered from the tip of an injection needle placed 12 mm from the apical root-end and an aspiration needle that was connected to a Root ZX apex locator placed 2 and 3 mm short of the apical root-end in groups 1 and 2, respectively. In the conventional method, the tip of an injection needle used for delivery of the irrigant and as an active electrode was placed 2 and 3 mm short of the apical root-end in groups 3 and 4, respectively, the tip of the aspiration needle was placed 12 mm from the apical root-end in these groups. The readings of the Root ZX during irrigation were recorded. The cleanliness of the canal was evaluated by scoring smear layer from scanning electron microscopy (SEM) images of the canal. Extrusion of NaOCl was detected by measuring the discoloured area of the agar around the apical root-end. The data obtained were statistically analysed by one-way anova, the Kruskal-Wallis test and Friedman's test. RESULTS: In the SEM study, the canals in groups 1-3 were significantly cleaner than those in the control and group 4 (P < 0.05). The mean Root ZX readings in groups 1-3 were approximately "0.5". The discoloured area in group 3 was significantly larger than the other groups (P < 0.05). CONCLUSIONS: Irrigation using the intracanal aspiration technique allowed more effective removal of the smear layer than that performed by the conventional method in an apically resected canine tooth. The intracanal aspiration technique produced limited extrusion of the irrigant beyond the apical foramen.

The role of mast cells in the development of 2, 4, 6-trinitrobenzene sulfonic acid-induced colitis in rats.

BACKGROUND: The role of mast cells in Crohn disease (CD) remains to be established. The aim of this study was to elucidate this in the development of CD-like colitis in rats by the use of mast-cell-deficient Ws/Ws and their control W+/W+ rats. METHODS: CD-like colitis was induced in both groups by an enema of 10 mg of 2,4, 6-trinitrobenzene sulfonic acid (TNBS) in 50% ethanol. Colonic damage, adhesion and colonic weight were measured at 7 and 14 days after the TNBS/ethanol enema. Rat mast cell protease-2 (RMCP-2) in the colonic tissue was also measured at 7 days after the enema. RESULTS: There was no significant difference between W+/W+ and Ws/Ws rats in terms of colonic damage, adhesion or colonic weight. The tissue content of RMCP-2 in Ws/Ws rats treated with either saline or TNBS/ethanol was only maintained at a much lower level than that in W+/W+ rats with the corresponding treatment. CONCLUSIONS: These results demonstrate that mast cells are not essential in the development of 2, 4, 6-trinitrobenzene sulfonic acid-induced colitis in rats.

Liver injury suppressing compounds from avocado (Persea americana).

To evaluate the protective activity of fruits against liver injury, 22 different fruits were fed to rats with liver damage caused by D-galactosamine, a powerful liver toxin. As measured by changes in the levels of plasma alanine aminotransferase (ALT) and aspartate aminotransferase (AST), avocado showed extraordinarily potent liver injury suppressing activity. Five active compounds were isolated and their structures determined. These were all fatty acid derivatives, of which three, namely, (2E,5E,12Z,15Z)-1-hydroxyheneicosa-2,5,12,15-tetraen-4-one, (2E,12Z,15Z)-1-hydroxyheneicosa-2,12,15-trien-4-one, and (5E,12Z)-2-hydroxy-4-oxoheneicosa-5,12-dien-1-yl acetate, were novel.

Comparison of the mode of action of ras p21 with those of protein kinases A and C in the stimulation of gene expression in NIH/3T3 cells.

To compare the mode of action of ras p21 with those of protein kinases A and C in the regulation of gene expression in NIH/3T3 cells, we investigated the transcriptional activity of various enhancer/promoters and enhancer motifs in the cells transfected with the c-Ha-rasva112 complementary DNA (cDNA). The results indicate that the c-Ha-rasva112 protein stimulates the enhancer/promoters of the c-fos gene, the metallothionein IIA gene, the simian virus 40 (SV40) virus genome and the Rous sarcoma (RS) virus genome, and the serum-response element and the 12-O-tetradecanoylphorbol-13-acetate (TPA)-response element in a manner independent of protein kinases A and C in NIH/3T3 cells.

Activation of the c-fos serum-response element by the activated c-Ha-ras protein in a manner independent of protein kinase C and cAMP-dependent protein kinase.

12-O-Tetradecanoylphorbol-13-acetate (TPA) activated the c-fos gene enhancer linked to the chloramphenicol acetyltransferase or luciferase reporter gene in the wild type PC-12 cells but not in the variant PC-12 cells that originated from the wild type cells. Transfection of the c-Ha-rasval12 complementary DNA (cDNA) or addition of dibutyryl cAMP to the wild type PC-12 cells as well as to the variant PC-12 cells activated the c-fos gene enhancer. Prolonged treatment of the wild type PC-12 cells with phorbol-12,13-dibutyrate caused down-regulation of protein kinase C. In these cells, TPA did not stimulate the c-fos gene enhancer any more, but transfection of the c-Ha-rasval12 cDNA still stimulated the c-fos gene enhancer to the same extent as induced in the control cells. Transfection of the c-Ha-rasval12 cDNA or addition of TPA to the wild type PC-12 cells stimulated the serum-response element but not the cAMP-response element. Dibutyryl cAMP stimulated both the serum-response element and the cAMP-response element in the wild type PC-12 cells. These results indicate that the c-Ha-rasval12 protein activates the serum-response element, but not the cAMP-response element in the c-fos gene enhancer, and that the signal pathway from the c-Ha-rasval12 protein to the c-fos serum-response element is independent of protein kinase C and cAMP-dependent protein kinase.