Applications of hydrodynamic models for modeling drifting jellyfish blooms around the Maltese Islands

Within the ambit of the MED-JELLYRISK project, the IOI-Malta Operational Centre is coordinating the development of a jellyfish dispersion model capable of generating both a hindcast and a forecast (extending up to a maximum of 4 days following day of sighting) output for the dispersion trajectory taken by a jellyfish bloom of specified densities and sighted at a specified location. The numerical tool is based on a high resolution hydrodynamic finite element coastal ocean model (SHYFEM) coupled with a particles tracking lagrangian model for reproducing both the surface water circulation and the transport and diffusion of numerical particles inside the area of interest. The coastal model is nested into an Open Ocean sub-regional 3D hydrodynamic model (ROSARIO), having a resolution of 1/640 and which reproduces daily the 3D hydrodynamic fields needed for predicting the fate of released numerical particles. The model domain was reproduced by means of a finite element mesh that was designed to accurately reproduce both the bathymetric features and the complex geometry of the Maltese archipelago coastlines. The system will be integrated into a Graphical User Interface (GUI) which will allow the user to define the position in time and space of a hypothetical bloom found in the Maltese waters, to select the amount of particles to simulate the jellyfish biomass and to launch the trajectory model run. The model will be partly validated by using the trajectories followed by a series of open water and coastal water drifters whose dispersion is geo-referenced and which have been regularly released by the IOI-MOC within Maltese coastal waters.peer-reviewe

The role of cellular fibronectin in the interaction of human endothelial cells with polymers

During in-vitro adhesion, spreading and proliferation of human endothelial cells (HEC) on tissue culture polystyrene (TCPS), cellular fibronectin is deposited onto the surface of TCPS in spite of the fact that relatively large amounts of proteins have been adsorbed from the serum-containing culture medium to this surface. Evidence is presented that serum proteins, adsorbed to the TCPS surface, are displaced by cellular fibronectin. In addition, the interaction of HEC with polyethylene, precoated with monoclonal antibodies directed against HEC membrane antigens and against extracellular matrix compounds, was studied. F(ab')2 fragments of two monoclonal antibodies were also included in this study. Preadsorption of these antibodies and F(ab')2 fragments resulted in cell adhesion and spreading as well as moderate cell proliferation (or no proliferation) for several days. A good cell proliferation of HEC was only observed on polyethylene precoated with fibronectin or an antibody directed against fibronectin. The results indicate that the direct or indirect deposition of fibronectin is a prerequisite for the proliferation of HEC. It is suggested that fibronectin, bound to a solid substrate, provides a biochemical signal necessary for the proliferation of HEC

No alternative to proliferation

We reflect on the nature, role and limits of non-empirical theory assessment in fundamental physics, focusing in particular on quantum gravity. We argue for the usefulness and, to some extent, necessity of non-empirical theory assessment, but also examine critically its dangers. We conclude that the principle of proliferation of theories is not only at the very root of theory assessment but all the more necessary when experimental tests are scarce, and also that, in the same situation, it represents the only medicine against the degeneration of scientific research programmes.Comment: 15 pages; contribution to the volume "Why trust a theory?", edited by: R. Dardashti, R. Dawid, K. Thebault, to be published by Cambridge University Pres

Skin Cell Proliferation Stimulated by Microneedles

A classical wound may be defined as a disruption of tissue integrity. Wounds, caused by trauma from accidents or surgery, that close via secondary intention rely on the biological phases of healing, i.e., hemostasis, inflammation, proliferation, and remodeling (HIPR). Depending on the wound type and severity, the inflammation phase begins immediately after injury and may last for an average of 7–14 days. Concurrent with the inflammation phase or slightly delayed, cell proliferation is stimulated followed by the activation of the remodeling (maturation) phase. The latter phase can last as long as 1 year or more, and the final healed state is represented by a scar tissue, a cross-linked collagen formation that usually aligns collagen fibers in a single direction. One may assume that skin microneedling that involves the use of dozens or as many as 200 needles that limit penetration to 1.5 mm over 1 cm2 of skin would cause trauma and bleeding followed by the classical HIPR. However, this is not the case or at least the HIPR phases are significantly curtailed and healing never ends in a scar formation. Conversely dermabrasion used in aesthetic medicine for improving skin quality is based on “ablation” (destruction or wounding of superficial skin layers), which requires several weeks for healing that involves formation of new skin layers. Such procedures provoke an acute inflammatory response. We believe that a less intense inflammatory response occurs following microneedle perforation of the skin. However, the mechanism of action of microneedling appears to be different. Here we review the potential mechanisms by which microneedling of the skin facilitates skin repair without scarring after the treatment of superficial burns, acne, hyperpigmentation, and the non-advancing periwound skin surrounding the chronic ulcerations of the integument

A characterization of four B16 murine melanoma cell sublines molecular fingerprint and proliferation behavior

Background: One of the most popular and versatile model of murine melanoma is by inoculating B16 cells in the syngeneic C57BL6J mouse strain. A characterization of different B16 modified cell sub-lines will be of real practical interest. For this aim, modern analytical tools like surface enhanced Raman spectroscopy/scattering (SERS) and MTT were employed to characterize both chemical composition and proliferation behavior of the selected cells. Methods: High quality SERS signal was recorded from each of the four types of B16 cell sub-lines: B164A5, B16GMCSF, B16FLT3, B16F10, in order to observe the differences between a parent cell line (B164A5) and other derived B16 cell sub-lines. Cells were incubated with silver nanoparticles of 50–100 nm diameter and the nanoparticles uptake inside the cells cytoplasm was proved by transmission electron microscopy (TEM) investigations. In order to characterize proliferation, growth curves of the four B16 cell lines, using different cell numbers and FCS concentration were obtained employing the MTT proliferation assay. For correlations doubling time were calculated. Results: SERS bands allowed the identification inside the cells of the main bio-molecular components such as: proteins, nucleic acids, and lipids. An "on and off" SERS effect was constantly present, which may be explained in terms of the employed laser power, as well as the possible different orientations of the adsorbed species in the cells in respect to the Ag nanoparticles. MTT results showed that among the four tested cell sub-lines B16 F10 is the most proliferative and B164A5 has the lower growth capacity. Regarding B16FLT3 cells and B16GMCSF cells, they present proliferation ability in between with slight slower potency for B16GMCSF cells. Conclusion: Molecular fingerprint and proliferation behavior of four B16 melanoma cell sub-lines were elucidated by associating SERS investigations with MTT proliferation assay

Nitric oxide from inflammatory origin impairs neural stem cell proliferation by inhibiting epidermal growth factor receptor signaling

Neuroinflammation is characterized by activation of microglial cells, followed by production of nitric oxide (NO), which may have different outcomes on neurogenesis, favoring or inhibiting this process. In the present study, we investigated how the inflammatory mediator NO can affect proliferation of neural stem cells (NSCs), and explored possible mechanisms underlying this effect. We investigated which mechanisms are involved in the regulation of NSC proliferation following treatment with an inflammatory stimulus (lipopolysaccharide plus IFN-gamma), using a culture system of subventricular zone (SVZ)-derived NSCs mixed with microglia cells obtained from wild-type mice (iNOS(+/+)) or from iNOS knockout mice (iNOS(-/-)). We found an impairment of NSC cell proliferation in iNOS(+/+) mixed cultures, which was not observed in iNOS(-/-) mixed cultures. Furthermore, the increased release of NO by activated iNOS(+/+) microglial cells decreased the activation of the ERK/MAPK signaling pathway, which was concomitant with an enhanced nitration of the EGF receptor. Preventing nitrogen reactive species formation with MnTBAP, a scavenger of peroxynitrite (ONOO-), or using the ONOO- degradation catalyst FeTMPyP cell proliferation and ERK signaling were restored to basal levels in iNOS(+/+) mixed cultures. Moreover, exposure to the NO donor NOC-18 (100 mu M), for 48 h, inhibited SVZ-derived NSC proliferation. Regarding the antiproliferative effect of NO, we found that NOC-18 caused the impairment of signaling through the ERK/MAPK pathway, which may be related to increased nitration of the EGF receptor in NSC. Using MnTBAP nitration was prevented, maintaining ERK signaling, rescuing NSC proliferation. We show that NO from inflammatory origin leads to a decreased function of the EGF receptor, which compromised proliferation of NSC. We also demonstrated that NO-mediated nitration of the EGF receptor caused a decrease in its phosphorylation, thus preventing regular proliferation signaling through the ERK/MAPK pathway.Foundation for Science and Technology, (FCT, Portugal); COMPETE; FEDER [PEst-C/SAU/LA0001/2013-2014, PEst-OE/EQB/LA0023/2013-2014, PTDC/SAU-NEU/102612/2008, PTDC/NEU-OSD/0473/2012]; FCT, Portugal [SERH/BPD/78901/2011, SERH/BD/38127/2007, SFRH/BD/77903/2011, SFRH/BD/79308/2011]info:eu-repo/semantics/publishedVersio

Inhibition of Tendon Cell Proliferation and Matrix Glycosaminoglycan Synthesis by Non-Steroidal Anti-Inflammatory Drugs in vitro

The purpose of this study was to investigate the effects of some commonly used non-steroidal anti-inflammatory drugs (NSAIDs) on human tendon. Explants of human digital flexor and patella tendons were cultured in medium containing pharmacological concentrations of NSAIDs. Cell proliferation was measured by incorporation of 3H-thymidine and glycosaminoglycan synthesis was measured by incorporation of 35S-Sulphate. Diclofenac and aceclofenac had no significant effect either on tendon cell proliferation or glycosaminoglycan synthesis. Indomethacin and naproxen inhibited cell proliferation in patella tendons and inhibited glycosaminoglycan synthesis in both digital flexor and patella tendons. If applicable to the in vivo situation, these NSAIDs should be used with caution in the treatment of pain after tendon injury and surgery