Utilizing Colored Dissolved Organic Matter to Derive Dissolved Black Carbon Export by Arctic Rivers

Wildfires have produced black carbon (BC) since land plants emerged. Condensed aromatic compounds, a form of BC, have accumulated to become a major component of the soil carbon pool. Condensed aromatics leach from soils into rivers, where they are termed dissolved black carbon (DBC). The transport of DBC by rivers to the sea is a major term in the global carbon and BC cycles. To estimate Arctic river DBC export, 25 samples collected from the six largest Arctic rivers (Kolyma, Lena, Mackenzie, Ob’, Yenisey and Yukon) were analyzed for dissolved organic carbon (DOC), colored dissolved organic matter (CDOM), and DBC. A simple, linear regression between DOC and DBC indicated that DBC accounted for 8.9 ± 0.3% DOC exported by Arctic rivers. To improve upon this estimate, an optical proxy for DBC was developed based upon the linear correlation between DBC concentrations and CDOM light absorption coefficients at 254 nm (a254). Relatively easy to measure a254 values were determined for 410 Arctic river samples between 2004 and 2010. Each of these a254 values was converted to a DBC concentration based upon the linear correlation, providing an extended record of DBC concentration. The extended DBC record was coupled with daily discharge data from the six rivers to estimate riverine DBC loads using the LOADEST modeling program. The six rivers studied cover 53% of the pan-Arctic watershed and exported 1.5 ± 0.1 million tons of DBC per year. Scaling up to the full area of the pan-Arctic watershed, we estimate that Arctic rivers carry 2.8 ± 0.3 million tons of DBC from land to the Arctic Ocean each year. This equates to ~8% of Arctic river DOC export, slightly less than indicated by the simpler DBC vs DOC correlation-based estimate. Riverine discharge is predicted to increase in a warmer Arctic. DBC export was positively correlated with river runoff, suggesting that the export of soil BC to the Arctic Ocean is likely to increase as the Arctic warms

Comparison of Engineering Wake Models with CFD Simulations

The engineering wake models by Jensen [1] and Frandsen et al. [2] are assessed for different scenarios simulated using Large Eddy Simulation and the Actuator Line method implemented in the Navier-Stokes equations. The scenarios include the far wake behind a single wind turbine, a long row of turbines in an atmospheric boundary layer, idealised cases of an infinitely long row of wind turbines and infinite wind farms with three different spacings. Both models include a wake expansion factor, which is calibrated to fit the simulated wake velocities. The analysis highlights physical deficiencies in the ability of the models to universally predict the wake velocities, as the expansion factor can be fitted for a given case, but with not apparent transition between the cases. 1

Assessing the carcinogenic potential of low-dose exposures to chemical mixtures in the environment: the challenge ahead.

Lifestyle factors are responsible for a considerable portion of cancer incidence worldwide, but credible estimates from the World Health Organization and the International Agency for Research on Cancer (IARC) suggest that the fraction of cancers attributable to toxic environmental exposures is between 7% and 19%. To explore the hypothesis that low-dose exposures to mixtures of chemicals in the environment may be combining to contribute to environmental carcinogenesis, we reviewed 11 hallmark phenotypes of cancer, multiple priority target sites for disruption in each area and prototypical chemical disruptors for all targets, this included dose-response characterizations, evidence of low-dose effects and cross-hallmark effects for all targets and chemicals. In total, 85 examples of chemicals were reviewed for actions on key pathways/mechanisms related to carcinogenesis. Only 15% (13/85) were found to have evidence of a dose-response threshold, whereas 59% (50/85) exerted low-dose effects. No dose-response information was found for the remaining 26% (22/85). Our analysis suggests that the cumulative effects of individual (non-carcinogenic) chemicals acting on different pathways, and a variety of related systems, organs, tissues and cells could plausibly conspire to produce carcinogenic synergies. Additional basic research on carcinogenesis and research focused on low-dose effects of chemical mixtures needs to be rigorously pursued before the merits of this hypothesis can be further advanced. However, the structure of the World Health Organization International Programme on Chemical Safety 'Mode of Action' framework should be revisited as it has inherent weaknesses that are not fully aligned with our current understanding of cancer biology

Carbon dioxide rebreathing in non-invasive ventilation. Analysis of masks, expiratory ports and ventilatory modes

Background and Aim. Carbon dioxide (CO2) rebreathing is a complication of non-invasive ventilation (NIV). Our objectives were to evaluate the ability of masks with exhaust vents (EV) to avoid rebreathing while using positive pressure (PP) NIV with different levels of expiratory pressure (EPAP). Concerning volume-cycled NIV, we aimed to determine whether cylindrical spacers located in the circuit generate rebreathing. Materials and methods. 5 healthy volunteers were evaluated. Bi-level PP was used with 3 nasal and 2 facial masks with and without EV. Spacers of increasing volume attached to nasal hermetic masks were evaluated with volume NIV. Inspired CO2 fraction was analyzed. Results. Rebreathing was zero with all nasal masks and EPAP levels. Using facial masks 1 volunteer showed rebreathing. There was no rebreathing while using all the spacers. Conclusions. In healthy volunteers, nasal and facial masks with EV prevent rebreathing. In addition, the use of spacers did not generate this undesirable phenomenon

Methylation screening of the TGFBI promoter in human lung and prostate cancer by methylation-specific PCR

<p>Abstract</p> <p>Background</p> <p>Hypermethylation of the <it>TGFBI </it>promoter has been shown to correlate with decreased expression of this gene in human tumor cell lines. In this study, we optimized a methylation-specific polymerase chain reaction (MSP) method and investigated the methylation status of the <it>TGFBI </it>promoter in human lung and prostate cancer specimens.</p> <p>Methods</p> <p>Methylation-specific primers were designed based on the methylation profiles of the <it>TGFBI </it>promoter in human tumor cell lines, and MSP conditions were optimized for accurate and efficient amplification. Genomic DNA was isolated from lung tumors and prostatectomy tissues of prostate cancer patients, bisulfite-converted, and analyzed by MSP.</p> <p>Results</p> <p>Among 50 lung cancer samples, 44.0% (22/50) harbored methylated CpG sites in the <it>TGFBI </it>promoter. An analysis correlating gene methylation status with clinicopathological cancer features revealed that dense methylation of the <it>TGFBI </it>promoter was associated with a metastatic phenotype, with 42.9% (6/14) of metastatic lung cancer samples demonstrating dense methylation vs. only 5.6% (2/36) of primary lung cancer samples (<it>p </it>< 0.05). Similar to these lung cancer results, 82.0% (41/50) of prostate cancer samples harbored methylated CpG sites in the <it>TGFBI </it>promoter, and dense methylation of the promoter was present in 38.9% (7/18) of prostate cancer samples with the feature of locoregional invasiveness vs. only 19.4% (6/31) of prostate cancer samples without locoregional invasiveness (<it>p </it>< 0.05). Furthermore, promoter hypermethylation correlated with highly reduced expression of the <it>TGFBI </it>gene in human lung and prostate tumor cell lines.</p> <p>Conclusion</p> <p>We successfully optimized a MSP method for the precise and efficient screening of <it>TGFBI </it>promoter methylation status. Dense methylation of the <it>TGFBI </it>promoter correlated with the extent of <it>TGFBI </it>gene silencing in tumor cell lines and was related to invasiveness of prostate tumors and metastatic status of lung cancer tumors. Thus, <it>TGFBI </it>promoter methylation can be used as a potential prognostic marker for invasiveness and metastasis in prostate and lung cancer patients, respectively.</p

A Fast Panel Code for Complex Actuator Disk Flows

A fast, linear scaling vortex method is presented to study inviscid incompressible flow problems involving one or more actuator disks. Building upon previous efforts that were limited to axi-symmetric flow cases, the proposed methodology is able to handle arbitrary configurations with no symmetry constraints. Applications include the conceptual study of wake interaction mechanisms in wind farms, and the correction of wind tunnel blockage effects in test sections of arbitrary shape. Actuator disks represent wind turbines through the shedding of a deformable vortex wake, discretized with a plaid of triangular distributed dipole singularities. An iterative method is adopted to align the wake with the local flow field, which is reconstructed from the vorticity field with a Green function approach. Interactions are computed with a Fast Multipole Method (FMM), effectively overcoming the quadratic scaling of computational time associated with traditional panel methods. When compared to direct computation, the use of an FMM algorithm reduced solution time by a factor 30 when studying the wake of a single actuator disk with 60000 panels. In the same case, the mass flux of the actuator streamtube was conserved to 0:002%. Finally, the presence of round and square impermeable walls around the actuator is considered to demonstrate the code applicability to wind tunnel wall interference correction problems

Mechanisms of environmental chemicals that enable the cancer hallmark of evasion of growth suppression

As part of the Halifax Project, this review brings attention to the potential effects of environmental chemicals on important molecular and cellular regulators of the cancer hallmark of evading growth suppression. Specifically, we review the mechanisms by which cancer cells escape the growth-inhibitory signals of p53, retinoblastoma protein, transforming growth factor-beta, gap junctions and contact inhibition. We discuss the effects of selected environmental chemicals on these mechanisms of growth inhibition and cross-reference the effects of these chemicals in other classical cancer hallmarks

Mechanisms of environmental chemicals that enable the cancer hallmark of evasion of growth suppression

As part of the Halifax Project, this review brings attention to the potential effects of environmental chemicals on important molecular and cellular regulators of the cancer hallmark of evading growth suppression. Specifically, we review the mechanisms by which cancer cells escape the growth-inhibitory signals of p53, retinoblastoma protein, transforming growth factor-beta, gap junctions and contact inhibition. We discuss the effects of selected environmental chemicals on these mechanisms of growth inhibition and cross-reference the effects of these chemicals in other classical cancer hallmarks.This is the publisher’s final pdf. The published article is copyrighted by the author(s) and published by Oxford University Press. The published article can be found at: http://carcin.oxfordjournals.org/. The publisher and the author(s) have made this article open access