Impact of natural (waves and currents) and anthropogenic (trawl) resuspension on the export of particulate matter to the open ocean: Application to the Gulf of Lion (NW Mediterranean)

Accepted manuscript version. Published version available at https://doi.org/10.1016/j.csr.2008.02.002. Licensed CC BY-NC-ND 4.0.Modern sediment deposits on continental margins form a vast reservoir of particulate matter that is regularly affected by resuspension processes. Resuspension by bottom trawling on shelves with strong fishing activity can modify the scale of natural disturbance by waves and currents. Recent field data show that the impact of bottom trawls on fine sediment resuspension per unit surface is comparable with that of the largest storms. We assessed the impact of both natural and anthropogenic processes on the dispersal of riverborne particles and shelf sediments on the Gulf of Lion shelf. We performed realistic numerical simulations of resuspension and transport forced by currents and waves or by a fleet of bottom trawlers. Simulations were conducted for a 16-month period (January 1998–April 1999) to characterise the seasonal variability. The sediment dynamics takes into account bed armoring, ripple geometry and the cohesive and non-cohesive characteristics of the sediments. Essential but uncertain parameters (clay content, erosion fluxes and critical shear stress for cohesive sediment) were set with existing data. Resuspension by waves and currents was controlled by shear stress, whereas resuspension by trawls was controlled by density and distribution of the bottom trawler fleet. Natural resuspension by waves and currents mostly occurred during short seasonal episodes, and was concentrated on the inner shelf. Trawling-induced resuspension, in contrast, occurred regularly throughout the year and was concentrated on the outer shelf. The total annual erosion by trawls (5.6×106 t y−1, t for metric tonnes) was four orders of magnitude lower than the erosion induced by waves and currents (35.3×109 t y−1). However the net resuspension (erosion/deposition budget) for trawling (0.4×106 t y−1) was only one order of magnitude lower than that for waves and currents (9.2×106 t y−1). Off-shelf export concerned the finest fraction of the sediment (clays and fine silts) and took place primarily at the southwestern end of the Gulf. Off-shelf transport was favoured during the winter 1999 by a very intense episode of dense shelf water cascading. Export of sediment resuspended by trawls (0.4×106 t y−1) was one order of magnitude lower than export associated with natural resuspension (8.5×106 t y−1). Trawling-induced resuspension is thought to represent one-third of the total export of suspended sediment from the shelf. A simulation combining both resuspension processes reveals no significant changes in resuspension and export rates compared with the sum of each individual process, suggesting the absence of interference between both processes.</p

Local and global Fokker-Planck neoclassical calculations showing flow and bootstrap current modification in a pedestal

In transport barriers, particularly H-mode edge pedestals, radial scale lengths can become comparable to the ion orbit width, causing neoclassical physics to become radially nonlocal. In this work, the resulting changes to neoclassical flow and current are examined both analytically and numerically. Steep density gradients are considered, with scale lengths comparable to the poloidal ion gyroradius, together with strong radial electric fields sufficient to electrostatically confine the ions. Attention is restricted to relatively weak ion temperature gradients (but permitting arbitrary electron temperature gradients), since in this limit a delta-f (small departures from a Maxwellian distribution) rather than full-f approach is justified. This assumption is in fact consistent with measured inter-ELM H-Mode edge pedestal density and ion temperature profiles in many present experiments, and is expected to be increasingly valid in future lower collisionality experiments. In the numerical analysis, the distribution function and Rosenbluth potentials are solved for simultaneously, allowing use of the exact field term in the linearized Fokker-Planck collision operator. In the pedestal, the parallel and poloidal flows are found to deviate strongly from the best available conventional neoclassical prediction, with large poloidal variation of a different form than in the local theory. These predicted effects may be observable experimentally. In the local limit, the Sauter bootstrap current formulae appear accurate at low collisionality, but they can overestimate the bootstrap current near the plateau regime. In the pedestal ordering, ion contributions to the bootstrap and Pfirsch-Schluter currents are also modified

Characterization of MCF mammary epithelial cells overexpressing the Arylhydrocarbon receptor (AhR)

<p>Abstract</p> <p>Background</p> <p>Recent reports indicate the existence of breast cancer cells expressing very high levels of the Arylhydrocarbon receptor (AhR), a ubiquitous intracellular receptor best known for mediating toxic action of dioxin and related pollutants. Positive correlation between the degree of AhR overexpression and states of increasing transformation of mammary epithelial cells appears to occur in the absence of any exogenous AhR ligands. These observations have raised many questions such as why and how AhR is overexpressed in breast cancer and its physiological roles in the progression to advanced carcinogenic transformation. To address those questions, we hypothesized that AhR overexpression occurs in cells experiencing deficiencies in normally required estrogen receptor (ER) signaling, and the basic role of AhR in such cases is to guide the affected cells to develop orchestrated cellular changes aimed at substituting the normal functions of ER. At the same time, the AhR serves as the mediator of the cell survival program in the absence of ER signaling.</p> <p>Methods</p> <p>We subjected two lines of Michigan Cancer Foundation (MCF) mammary epithelial cells to 3 different types ER interacting agents for a number of passages and followed the changes in the expression of AhR mRNA. The resulting sublines were analyzed for phenotypical changes and unique molecular characteristics.</p> <p>Results</p> <p>MCF10AT1 cells continuously exposed to 17-beta-estradiol (E2) developed sub-lines that show AhR overexpression with the characteristic phenotype of increased proliferation, and distinct resistance to apoptosis. When these chemically selected cell lines were treated with a specific AhR antagonist, 3-methoxy-4-nitroflavone (MNF), both of the above abnormal cellular characteristics disappeared, indicating the pivotal role of AhR in expressing those cellular phenotypes. The most prominent molecular characteristics of these AhR overexpressing MCF cells were found to be overexpression of ErbB2 and COX-2. Furthermore, we could demonstrate that suppression of AhR functions through anti-AhR siRNA or MNF causes the recovery of ERalpha functions.</p> <p>Conclusion</p> <p>One of the main causes for AhR overexpression in these MCF breast cancer cells appears to be the loss of ERalpha functions. This phenomenon is likely to be based on the mutually antagonistic relationship between ER and AhR.</p

Genome wide SNP comparative analysis between EGFR and KRAS mutated NSCLC and characterization of two models of oncogenic cooperation in non-small cell lung carcinoma

<p>Abstract</p> <p>Background</p> <p>Lung cancer with EGFR mutation was shown to be a specific clinical entity. In order to better understand the biology behind this disease we used a genome wide characterization of loss of heterozygosity and amplification by Single Nucleotide Polymorphism (SNP) Array analysis to point out chromosome segments linked to <it>EGFR </it>mutations. To do so, we compared genetic profiles between <it>EGFR </it>mutated adenocarcinomas (ADC) and <it>KRAS </it>mutated ADC from 24 women with localized lung cancer.</p> <p>Results</p> <p>Patterns of alterations were different between <it>EGFR </it>and <it>KRAS </it>mutated tumors and specific chromosomes alterations were linked to the <it>EGFR </it>mutated group. Indeed chromosome regions 14q21.3 (p = 0.027), 7p21.3-p21.2 (p = 0.032), 7p21.3 (p = 0.042) and 7p21.2-7p15.3 (p = 0.043) were found significantly amplified in EGFR mutated tumors. Within those regions 3 genes are of special interest <it>ITGB8</it>, <it>HDAC9 </it>and <it>TWIST1</it>. Moreover, homozygous deletions at <it>CDKN2A </it>and LOH at <it>RB1 </it>were identified in <it>EGFR </it>mutated tumors. We therefore tested the existence of a link between EGFR mutation, CDKN2A homozygous deletion and cyclin amplification in a larger series of tumors. Indeed, in a series of non-small-cell lung carcinoma (n = 98) we showed that homozygous deletions at <it>CDKN2A </it>were linked to <it>EGFR </it>mutations and absence of smoking whereas cyclin amplifications (<it>CCNE1 </it>and <it>CCND1</it>) were associated to <it>TP53 </it>mutations and smoking habit.</p> <p>Conclusion</p> <p>All together, our results show that genome wide patterns of alteration differ between <it>EGFR </it>and <it>KRAS </it>mutated lung ADC, describe two models of oncogenic cooperation involving either <it>EGFR </it>mutation and <it>CDKN2A </it>deletion or cyclin amplification and <it>TP53 </it>inactivating mutations and identified new chromosome regions at 7p and 14q associated to EGFR mutations in lung cancer.</p

Citrullination of histone H3 drives IL-6 production by bone marrow mesenchymal stem cells in MGUS and multiple myeloma

Multiple myeloma (MM), an incurable plasma cell malignancy, requires localisation within the bone marrow. This microenvironment facilitates crucial interactions between the cancer cells and stromal cell types that permit the tumour to survival and proliferate. There is increasing evidence that the bone marrow mesenchymal stem cell (BMMSC) is stably altered in patients with MM – a phenotype also postulated to exist in patients with monoclonal gammopathy of undetermined significance (MGUS) a benign condition that precedes MM. In this study, we describe a mechanism by which increased expression of peptidyl arginine deiminase 2 (PADI2) by BMMSCs in patients with MGUS and MM directly alters malignant plasma cell phenotype. We identify PADI2 as one of the most highly upregulated transcripts in BMMSCs from both MGUS and MM patients, and that through its enzymatic deimination of histone H3 arginine 26, PADI2 activity directly induces the upregulation of interleukin-6 (IL-6) expression. This leads to the acquisition of resistance to the chemotherapeutic agent, bortezomib, by malignant plasma cells. We therefore describe a novel mechanism by which BMMSC dysfunction in patients with MGUS and MM directly leads to pro-malignancy signalling through the citrullination of histone H3R26

Characterization of an Orphan Diterpenoid Biosynthetic Operon from Salinispora arenicola

While more commonly associated with plants than microbes, diterpenoid natural products have been reported to have profound effects in marine microbe–microbe interactions. Intriguingly, the genome of the marine bacterium Salinispora arenicola CNS-205 contains a putative diterpenoid biosynthetic operon, terp1. Here recombinant expression studies are reported, indicating that this three-gene operon leads to the production of isopimara-8,15-dien-19-ol (4). Although 4 is not observed in pure cultures of S. arenicola, it is plausible that the terp1 operon is only expressed under certain physiologically relevant conditions such as in the presence of other marine organisms

A Defined Terminal Region of the E. coli Chromosome Shows Late Segregation and High FtsK Activity

Background: The FtsK DNA-translocase controls the last steps of chromosome segregation in E. coli. It translocates sister chromosomes using the KOPS DNA motifs to orient its activity, and controls the resolution of dimeric forms of sister chromosomes by XerCD-mediated recombination at the dif site and their decatenation by TopoIV. Methodology: We have used XerCD/dif recombination as a genetic trap to probe the interaction of FtsK with loci located in different regions of the chromosome. This assay revealed that the activity of FtsK is restricted to a,400 kb terminal region of the chromosome around the natural position of the dif site. Preferential interaction with this region required the tethering of FtsK to the division septum via its N-terminal domain as well as its translocation activity. However, the KOPSrecognition activity of FtsK was not required. Displacement of replication termination outside the FtsK high activity region had no effect on FtsK activity and deletion of a part of this region was not compensated by its extension to neighbouring regions. By observing the fate of fluorescent-tagged loci of the ter region, we found that segregation of the FtsK high activity region is delayed compared to that of its adjacent regions. Significance: Our results show that a restricted terminal region of the chromosome is specifically dedicated to the last step

Simultaneous detection of lung fusions using a multiplex RT-PCR next generation sequencing-based approach:A multi-institutional research study

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