Release of methacrylic acid from dental composites.

OBJECTIVE: The aim of this study was to investigate the release of methacrylic acid from four commercial dental composite restoratives (Silux Plus (3M), Z100 (3M), Ariston pHc (Vivadent) and Surefil (Dentsply)). METHODS: Three specimen disks (10(0.2) mm in diameter and 2(0.2) mm thick), were prepared for each material using custom-made molds. Each disk was placed in artificial saliva for 24 h at 37 degrees C, rinsed and subsequently immersed in 1.5 ml of deionised water in an airtight glass container. The container was continuously shaken at a speed of 80 rpm for 24 h at 37 degrees C in an orbital incubator. After 24 h (Day 1), the water was removed and analyzed. The specimen disk was then re-immersed into another 1.5 ml of fresh deionised water. The procedure of removing and refilling of the water was repeated for a total of 7 days. The sample solutions were filtered and injected into the capillary electrophoresis system for analysis immediately after collection. Statistical analysis was performed by ANOVA and Scheffe's test. RESULTS: For Days 1-7, methacrylic acid released in water at 37 degrees C by Ariston was significantly greater than that of the other composites. Ranking from least to greatest total (cumulative over 7 days) methacrylic acid release was as follows: Z100 (5.66 ppm) < Silux (8.81 ppm) < Surefil (20.21 ppm) < Ariston (519.04 ppm). Methacrylic acid release was greatest at Day 1 for all materials and generally decreased with time. SIGNIFICANCE: Some composites may release high levels of methacrylic acid. The biological effects of such high levels of methacrylic acid is not known and warrant further in vivo and in vitro investigations.     

Distal fingertip replantation without skeletal fixation

The replantation of fingertip amputation (through the nail bed) requires repair of the artery and vein on the palmar side. These structures are present in different planes, with the artery being deeper and the veins superficial. The authors believe that vascular repair in such cases is facilitated by stabilization of the amputated part by nail-bed repair alone. This provides a certain degree of flexibility, which allows for easier placement of clamps in the limited space available. Although Kirschner wires were not used for bony fixation, bony union was achieved in all five cases in which this technique was used.     

Trp53-dependent DNA-repair is affected by the codon 72 polymorphism

Trp53 is arguably the most critical tumour suppressor gene product that inhibits malignant transformation. Besides mutations that inactivate Trp53 functions, genetic polymorphisms have been suggested to be risk factors for cancer. A polymorphic site at codon 72 in exon 4 encodes either an arginine amino acid (Trp53(72R)) or a proline residue (Trp53(72P)). Previous studies have shown that the Trp53(72R) form is more efficient in apoptosis induction, whereas the Trp53(72P) form was suggested to induce G1 arrest better. Here we report that Trp53(72P) is more efficient than Trp53(72R) in specifically activating several Trp53-dependent DNA-repair target genes in several cellular systems. Moreover, using isogenic cell lines and several DNA-repair assays, we show that Trp53(72P) cells have a significantly higher DNA-repair capacity than the Trp53(72R) cells. Furthermore, Trp53(72P)-expressing cells exhibit reduced micronuclei formation compared to Trp53(72R)-expressing cells, suggesting that genomic instability is reduced in these cells. Together, the data highlight the functional differences between the Trp53 polymorphic variants, and suggest that their expression status may influence cancer risk.     

The tumour-suppressor p53 is not required for pancreatic beta cell death during diabetes and upon irradiation.

Immune-independent diabetes often occurs via pancreatic beta cell dysfunction. However, the role of the tumour suppressor p53 that regulates cellular life and death in multiple tissues, in pancreatic cell death and diabetes has not been clarified. We have therefore utilized an established mouse model for diabetes in which the MHC class I antigen is overexpressed in pancreatic beta cells under the rat insulin promoter, to investigate the role of p53. We show that pancreatic beta cell death, as determined by TUNEL staining, is elevated in transgenic mice compared to wild-type mice. However, there was no increase in immuno-reactivity towards anti-p53 antibodies in the pancreas of transgenic mice over the course of diabetes formation and beta cell death, suggesting that p53 may not be involved in these processes. Interestingly, p53 expression was also not induced in pancreas upon gamma-irradiation, which resulted in a massive increase in the number of TUNEL-positive cells, suggesting that the p53 pathway may not be causally involved in pancreatic cell death. To further confirm these findings, we generated MHC class I transgenic mice lacking p53 expression. Absence of p53 did not result in any significant changes in pancreatic morphology or affect cell death levels. Importantly, p53 absence did not rescue the diabetic phenotype of the transgenic mice. The results therefore demonstrate that p53 may not be causally involved in pancreatic beta cell death, and suggests that the classical cell death pathway dependent on p53 may not be operating in pancreatic beta cells.