Micronuclei induced by airborne particulate matter from Mexico City

Particulate air pollution is an important environmental health risk. In the present study, we have investigated the ability of chemically characterized water and organic-soluble extracts of PM(10) from two different regions of Mexico City to induce micronuclei in a human epithelial cell line. We also evaluated the association between the chemical characteristics of the PM and its genotoxicity. The airborne particulate samples were collected from an industrial and a residential region; a Hi-Vol air sampler was used to collect PM(10) on glass fiber filters. PM mass was determined by gravimetric analysis of the filters. One section of each PM(10) filter was agitated either with deionized water to extract water-soluble compounds or with dichloromethane to prepare organic-soluble compounds. The chemical composition of the extracts was determined by ion and gas chromatography and atomic adsorption spectroscopy. A549-human alveolar epithelial cells were exposed to different concentrations of PM(10) extracts and the cytokinesis blocked micronucleus assay was performed to measure DNA damage. Even though the industrial region had a higher PM concentration, higher amounts of metals and PAHs were found in the residential area. Both industrial and residential extracts induced a significant concentration-related increase in the micronuclei frequency. The PM(10) water-soluble industrial extract induced significantly more micronuclei than the one of the residential region; inversely, the organic residential extract induced more micronuclei than the one from the industrial region. The association between the induction of micronuclei and the chemical components obtained by the comparative analysis of standardized regression coefficients showed that cadmium and PAHs were significantly associated with micronuclei induction. Data indicate that water-soluble metals and the organic-soluble fraction of PM(10) are both important in the production of micronuclei. Effects observed, point to the risk of PM exposure and shows the need of integrative studies.     

Nuclear translocation of β-catenin during mesenchymal stem cells differentiation into hepatocytes is associated with a tumoral phenotype

Wnt/β-catenin pathway controls biochemical processes related to cell differentiation. In committed cells the alteration of this pathway has been associated with tumors as hepatocellular carcinoma or hepatoblastoma. The present study evaluated the role of Wnt/β-catenin activation during human mesenchymal stem cells differentiation into hepatocytes. The differentiation to hepatocytes was achieved by the addition of two different conditioned media. In one of them, β-catenin nuclear translocation, up-regulation of genes related to the Wnt/β-catenin pathway, such as Lrp5 and Fzd3, as well as the oncogenes c-myc and p53 were observed. While in the other protocol there was a Wnt/β-catenin inactivation. Hepatocytes with nuclear translocation of β-catenin also had abnormal cellular proliferation, and expressed membrane proteins involved in hepatocellular carcinoma, metastatic behavior and cancer stem cells. Further, these cells had also increased auto-renewal capability as shown in spheroids formation assay. Comparison of both differentiation protocols by 2D-DIGE proteomic analysis revealed differential expression of 11 proteins with altered expression in hepatocellular carcinoma. Cathepsin B and D, adenine phosphoribosyltransferase, triosephosphate isomerase, inorganic pyrophosphatase, peptidyl-prolyl cis-trans isomerase A or lactate dehydrogenase β-chain were up-regulated only with the protocol associated with Wnt signaling activation while other proteins involved in tumor suppression, such as transgelin or tropomyosin β-chain were down-regulated in this protocol. In conclusion, our results suggest that activation of the Wnt/β-catenin pathway during human mesenchymal stem cells differentiation into hepatocytes is associated with a tumoral phenotype.     

Reduction of bromate by biogenic sulfide produced during microbial sulfur disproportionation

Bromate (BrO₃ ⁻) is a carcinogenic contaminant formed during ozonation of waters that contain trace amounts of bromide. Previous research shows that bromate can be microbially reduced to bromide using organic (i.e. acetate, glucose, ethanol) and inorganic (H₂) electron-donating substrates. In this study, the reduction of bromate by a mixed microbial culture was investigated using elemental sulfur (S⁰) as an electron donor. In batch bioassays performed at 30°C, bromate (0.30 mM) was completely converted to bromide after 10 days and no accumulation of intermediates occurred. Bromate was also reduced in cultures supplemented with thiosulfate and hydrogen sulfide as electron donor. Our results demonstrated that S⁰-disproportionating microorganisms were responsible for the reduction of bromate in cultures spiked with S⁰ through an indirect mechanism involving microbial formation of sulfide and subsequent abiotic reduction of bromate by the biogenic sulfide. Confirmation of this mechanism is the fact that bromate was shown to undergo rapid chemical reduction by sulfide (but not S⁰ or thiosulfate) in abiotic experiments. Bromate concentrations above 0.30 mM inhibited sulfide formation by S⁰-disproportionating bacteria, leading to a decrease in the rate of bromate reduction. The results suggest that biological formation of sulfide from by S⁰ disproportionation could support the chemical removal of bromate without having to directly use sulfide as a reagent.     

A gold(I) complex with a vitamin K3 derivative: characterization and antitumoral activity

Reaction of the vitamin K(3) derivative menadione sodium bisulfite thiosemicarbazone (NaK(3)TSC) with chloro(triethylphosphine)gold(I) afforded the complex [AuPEt(3)(K(3)TSC)]. This compound consists of discrete molecules in which the metal is almost linearly coordinated to P and S. Preliminary in vitro screening showed significant anti-cancer activity, notably against the cisplatin-resistant cell line A2780cis.     

Disability transitions after 30 months in three community-dwelling diagnostic groups in Spain

Background

Little is known about changes in disability over time among community-dwelling patients. Accordingly, this study sought to assess medium-term disability transitions.

Patients and Methods

300 chronic obstructive pulmonary disease (COPD), chronic heart failure and stroke patients living at home in Madrid were selected from general practitioner lists. In 2009, disability was assessed after a mean of 30 months using the World Health Organisation (WHO) Disability Assessment Schedule 2.0 (WHODAS 2.0). Follow-up was completed using death registries. Losses to follow-up were due to: death, 56; institutionalisation, 9; non-location, 18; and non-participation, 17. Changes in WHODAS 2.0 scores and life status were described and analysed using Cox and multinomial regression. Disability at end of follow-up was imputed for 56 deceased and 44 surviving patients.

Results

Mean disability scores for 200 surviving patients at end of follow-up were similar to baseline scores for the whole group, higher than their own baseline scores, and rose by 16.3% when imputed values were added. The strongest Cox predictors of death were: age over 84 years, adjusted hazard ratios with 95%CI 8.18 (3.06-21.85); severe/complete vs. no/mild disability, 5.18 (0.68-39.48); and stroke compared to COPD, 1.40 (0.67-2.91). Non-participants and institutionalised patients had higher proportions with severe/complete baseline disability. A one-point change in baseline WHODAS 2.0 score predicted independent increases in risk of 12% (8%-15%) for severe/complete disability or death.

Conclusions

A considerably high proportion of community-dwelling patients diagnosed with COPD, CHF and stroke undergo medium-term changes in disability or vital status. The main features of the emerging pattern for this group appear to be as follows: approximately two-thirds of patients continue living at home with moderately reduced functional status; 1/3 die or worsen to severe/complete disability; and 1/10 improve. Baseline disability scores, age and diagnosis are associated with disability and death in the medium term.     

Analysis of several biomechanical models for the simulation of lamb liver behaviour using similarity coefficients from medical image

In this study, six biomechanical models for simulating lamb liver behaviour are presented. They are validated using similarity coefficients from Medical Image on reconstructed volumes from computerised tomography images. In particular, the Jaccard and Hausdorff coefficients are used. Loads of 20 and 40 g are applied to the livers and their deformation is simulated by means of the finite element method. The models used are a linear elastic model, a neo-Hookean model, a Mooney–Rivlin model, an Ogden model, a linear viscoelastic model and a viscohyperelastic model. The model that provided a behaviour that is closest to reality was the viscohyperelastic model, where the hyperelastic part was modelled with an Ogden model.