In vitro toxicity of formocresol, ferric sulphate, and grey MTA on human periodontal ligament fibroblasts.

AIM: This was to assess and compare the in vitro toxicity of formocresol, ferric sulphate and MTA on cultured human periodontal ligament (PDL) fibroblasts. STUDY DESIGN: PDL cells were obtained from sound first permanent molars and cultured in Dulbecco's modified Eagle's medium. METHODS: PDL cells were subjected to different concentrations of formocresol, ferric sulphate, and grey MTA for 24, 48, and 72 h at 37 °C. Cells that were not exposed to the tested materials served as the negative control. In vitro toxicity was assessed using MTT assay. STATISTICS: Statistical analysis of data was accomplished using ANOVA and Tukey statistical tests (p<0.05). RESULTS: The overall toxicity ranking of the tested materials was as follows: formocresol>ferric sulphate>grey MTA. Only grey MTA had comparable cell viability to the negative control, the other tested materials were significantly inferior at the three exposure periods (p<0.05). CONCLUSION: Regarding the viability of PDL fibroblasts, MTA stands as the most promising substitute to formocresol. However, considering MTA's unavailability and high price in Jordan, ferric sulphate may be the best alternative to formocresol in pulpotomy of primary teeth.

In vitro toxicity of grey MTA in comparison to white MTA on human periodontal ligament fibroblasts.

AIM: This was to define and compare the in vitro toxicity of grey MTA with that of white MTA on cultured human periodontal ligament (PDL) fibroblasts. METHODS: PDL cells were obtained from sound first permanent molars and cultured in Dulbecco's Modified Eagle's Medium. Cultures were subjected to different concentrations of grey and white MTA (0.5, 5, 50 and 500 µg/ml) for 24 h at 37 °C. Cells that were not exposed to grey or white MTA served as the negative control. In vitro toxicity was assessed using MTT assay. STATISTICS: The results were compared using ANOVA and Tukey statistical tests (p < 0.05). RESULTS: White MTA presented higher in vitro toxicity than grey MTA. However, the differences were almost insignificant (p > 0.05). CONCLUSION: Both colours of MTA are biocompatible since they were both able to preserve PDL fibroblasts for up to 24 h. MTA is as a promising alternative in pulpotomy of primary teeth.

Weed control in rice with metham-sodium.

Metam-sodium is a soil fumigant with herbicidal properties. A field experiment was conducted in 2000 at Copiano (Pavia, Italy) to determine the efficacy of three rates of metam-sodium (300, 450 and 600 l/ha) at three different planting times (5, 12 and 18 days after chemical treatments) for the control of weeds in rice cultivation. The study mainly focused on the control of red rice (Oryza sativa var. selvatica), a weed which is worldwide distributed in rice fields and difficult to eradicate Test design was a split-plot with four replications. The main plot size was 13, 5 by 15 m and the subplot size was 13, 5 by 5 m. The chemical treatments were carried out as pre-sowing. Two days after chemical treatments, all field plots were flooded with 10 cm of water as practiced locally. An early variety of rice (Loto) was sown at 150 kg/ha. Weed control was visually evaluated as a percentage of ground covering by all weeds and by each weed individually at three, four and five weeks after treatments. Observations were made also on rice selectivity, and rice grain yield was assessed at the end. Metam-sodium did not injure the rice plants. Metam-sodium at 450 l/ha controlled 100%, 97% and 92% of red rice at the first, second and third observations, respectively. Good results were also obtained with metam-sodium at 300 and 600 l/ha, which controlled 94 to 82% of red rice during the season. Echinochloa crus-galli was better controlled with the higher rates of metam-sodium, particularly in the early part of the season. Metam-sodium did not show enough efficacy in this study against Heteranthera reniformis, Bulboschoenus maritimus and Lindernia spp. The best rice grain yield was obtained with all rates of metam-sodium, when rice was sown 5 days after treatment.

Effects of water management and herbicide treatments on red rice control.

Two field experiments were conducted in 1999 and 2000 at Zeme (Pavia, Italy) to determine the effects of water managements and herbicide treatments on red rice control. In the first experiment, all plots were flooded 10-13 cm deep from April 1 to May 17 in 1999 and from April 3 to May 6 in 2000. At the same time, in the second experiment, the plots were alternately drained-flooded. At the end of water management, all plots of both experiments were drained and sprayed with herbicides to control the emerged red rice plants. In both years were applied: Propaquizafop 78 g a.i.ha-1, Cycloxydim at 300 and 400 g a.i. ha-1; Dalapon at 15.300 Kg a.i. ha-1; Quizalofop-ethyl at 100 g a.i. ha-1. Six days after the chemical treatments, all field plots were flooded 10 cm deep and three days later, an early variety of rice (Loto) was sown at 150 Kg ha-1. Seedling emergence was reduced by lack of oxygen (especially from seeds covered with soil in flooded condition). In alternately drained-flooded soil, the red rice emerged and developed from seeds located in the top 4-5 cm. In flooded condition, no red rice plants emerged from seeds at more than 1 cm depth. In both experiments, the density of red rice plants increased during the season in the untreated check and in the plots where treatments were ineffective or performed poorly. The best red rice control, both in submerged and in alternately drained-flooded soil, was obtained with Quizalofop-ethyl (100 g a.i./ha), Cycloxydim (300 and 400 g a.i.ha-1) and Propaquizafop (78 g a.i.ha-1). These herbicides controlled 90-99% of red rice. Partial control of red rice resulted with the other chemical treatments. The shattered grains of red rice were reduced in both experiments by the herbicide treatments. Grain yield reflected the level of red rice control. In fact, the highest commercial grain yields were obtained with Quizalofop-ethyl, Propaquizafop, and Cycloxydim (400 g a.i.ha-1), in both years and experiments. The red rice percentages of the total yields resulted about 3.6-5.7% with all chemical treatments except Dalapon, which was not much effective.

Modeling human congenital disorder of glycosylation type IIa in the mouse: conservation of asparagine-linked glycan-dependent functions in mammalian physiology and insights into disease pathogenesis.

The congenital disorders of glycosylation (CDGs) are recent additions to the repertoire of inherited human genetic diseases. Frequency of CDGs is unknown since most cases are believed to be misdiagnosed or unrecognized. With few patients identified and heterogeneity in disease signs noted, studies of animal models may provide increased understanding of pathogenic mechanisms. However, features of mammalian glycan biosynthesis and species-specific variations in glycan repertoires have cast doubt on whether animal models of human genetic defects in protein glycosylation will reproduce pathogenic events and disease signs. We have introduced a mutation into the mouse germline that recapitulates the glycan biosynthetic defect responsible for human CDG type IIa (CDG-IIa). Mice lacking the Mgat2 gene were deficient in GlcNAcT-II glycosyltransferase activity and complex N-glycans, resulting in severe gastrointestinal, hematologic, and osteogenic abnormalities. With use of a lectin-based diagnostic screen for CDG-IIa, we found that all Mgat2-null mice died in early postnatal development. However, crossing the Mgat2 mutation into a distinct genetic background resulted in a low frequency of survivors. Mice deficient in complex N-glycans exhibited most CDG-IIa disease signs; however, some signs were unique to the aged mouse or are prognostic in human CDG-IIa. Unexpectedly, analyses of N-glycan structures in Mgat2-null mice revealed a novel oligosaccharide branch on the "bisecting" N-acetylglucosamine. These genetic, biochemical, and physiologic studies indicate conserved functions for N-glycan branches produced in the Golgi apparatus among two mammalian species and suggest possible therapeutic approaches to GlcNAcT-II deficiency. Our findings indicate that human genetic disease due to aberrant protein glycosylation can be modeled in the mouse to gain insights into N-glycan-dependent physiology and the pathogenesis of CDG-IIa.