bcmca ca/document-library/) During the Marxan experts workshop,

bcmca.ca/document-library/). During the Marxan experts workshop, selleck chemicals a new tool called Marxan with Zones [12] was recommended for running analyses incorporating human use data. At

that time BCMCA decided it was not feasible to use Marxan with Zones due to the learning curve, time constraints and the unproven nature of the new tool. Instead, all the human use scenarios were designed to use Marxan to identify areas important to human use by exploring what happens to the footprint if uses were reduced. Targets for ecological features are intended to quantify the amount required to meet ecological objectives. At the ecological workshops, experts were requested to recommend a range

of targets for each feature, spanning a minimum to preferred amount selleck screening library (see Ban et al. [18] for details). Workshops were attended by regional species experts who drew upon their own experience and knowledge to recommend targets. Targets for physical classification and representation features were proposed by the Project Team and reviewed by experts. During data review, workshop experts and data providers were given a chance to view the collated spatial data, and were asked to review target recommendations and provide targets for any features lacking an established target range. Any targets still missing after the review were systematically assigned by the Project Team. An unanticipated result of asking experts to recommend targets through separate workshops was that values differed greatly among ecological themes (e.g., recommended seabirds targets differed from marine plant targets and invertebrate targets, etc). The BCMCA Project Team decided to illustrate solutions for three added “What if…?” scenarios using

consistent targets for features in all ecological themes. Target ranges for these scenarios were collaboratively set by the BCMCA Project Team after consulting best practices, peer-reviewed scientific literature and the advice of the ecological experts ( Fig. 1). Marxan scenarios were run using low, medium and high target values for Liothyronine Sodium both the expert-recommended and Project Team target ranges in order to visually display the impact that targets have on the footprint of the Marxan solutions. To incorporate human use features, the Project Team initially suggested running Marxan for ecological features, using human uses as a ‘cost’, as is commonly done in Marxan analyses [21]. Alternately, an option was to set targets for human use features, which tells Marxan how much of each feature to include in the solution (i.e., to identify areas of important for all human uses, as per [13]).

The slides were then washed in PBS and mounted Orthotopic U87ΔEG

The slides were then washed in PBS and mounted. Orthotopic U87ΔEGFR xenograft mouse models treated with bevacizumab or the combination of bevacizumab and cilengitide were killed at 18 days after tumor implantation (n = 3 per treatment). Approximately 40 mg of brain tumor samples were excised cleanly from each mouse, and RNA was extracted using TRIzol (Life Technologies, Carlsbad, CA) and an RNeasy Mini Kit (Qiagen, Venlo, Netherlands). They were analyzed

using a CodeLink Human Whole Genome Bioarray (Applied Microarrays, Inc, Tempe, AZ). We entrusted the microarray analyses to Filgen, Inc (Nagoya, Japan). Briefly, for each bioarray, 10 μg of biotin-labeled aRNA, which was prepared using a MessageAmp II-Biotin Enhanced Kit in a total volume of 25 μl, was added FK228 chemical structure to 5 μl of 5 × fragmentation buffer, which was then incubated at 94°C for 20 minutes. Thereafter, Ruxolitinib cost 10 μg of fragmented cRNA, 78 μl of hybridization buffer component A, and 130 μl of hybridization buffer component B were added, and the final volume was brought up to 260 μl with water. The resultant hybridization reaction mixture was incubated at

90°C for 5 minutes, after which 250 μl were slowly injected into the input port of each array, and the ports were sealed with sealing strips. The bioarrays were incubated for 18 hours at 37°C while shaking at 300 rpm. A consistent hybridization time was maintained for comparative experiments. Following the incubation, the bioarrays were washed with 0.75 Tris-NaCl-Tween (TNT) buffer Mannose-binding protein-associated serine protease (0.10 M Tris-HCl, pH 7.6, 0.15 M NaCl, 0.05% Tween 20) and incubated at 46°C for 1 hour. Each slot of the small reagent reservoir was then filled with 3.4 ml of Cy5-streptavidin working solution, and the array was incubated at 25°C for 30 minutes. Thereafter, the bioarrays were washed four times for 5 minutes each with 1 × TNT buffer at 25°C, rinsed twice in 0.1 × SSC

(Ambion, Austin, TX)/0.05% Tween 20 for 30 seconds each, and immediately dried by centrifugation for 3 minutes at 25°C. Finally, the arrays were scanned using a GenePix4000B Array Scanner (Molecular Devices, Sunnyvale, CA). A gene was defined as being upregulated when the combination therapy/bevacizumab monotherapy average intensity ratio was > 2.0, and downregulated when the combination therapy/bevacizumab monotherapy ratio was < 0.5. We performed pathway analysis on the genes with increased and decreased expression using Microarray Data Analysis Tool Ver3.2 (Filgen, Inc). The data were extracted using the following criteria: Z score > 0 and P value < .05. Total RNA was isolated from cultured U87ΔEGFR cells treated with cilengitide (1.0 μM for 16 hours) and untreated control U87ΔEGFR cells using an RNeasy Mini Kit (Qiagen, Hilden, Germany).

Many optimization methods have been proposed to solve inverse pro

Many optimization methods have been proposed to solve inverse problems, based on the estimation of deterministic and stochastic parameters. Among the deterministic methods, the Levenberg–Marquardt method has been used successfully in several

areas (Kanevce et al., 2005, Mejias et al., 2003 and Mendonça et al., 2005). Among the stochastic methods, the Differential Akt activation Evolution method has been applied less frequently to inverse problems, but has been used by Kanevce et al., 2005, Mariani and Coelho, 2009a, Mariani and Coelho, 2009b, Mariani et al., 2008 and da Silva et al., 2009. Optimization methods for estimating parameter are used to estimate the diffusion coefficient as a function of the minimization of J by the sum of squared differences between the experimental moisture content and the moisture content computed with a diffusion model: equation(5) J=∑1n(Xexp−Xcomp)2where Xexp is the experimental moisture content and Xcomp is the computed moisture content. A set of moisture contents was obtained experimentally

at discrete times during the unsteady drying process. The literature uses different criteria to evaluate the quality of the fit obtained by the mathematical see more model and optimization methods to simulate the experimental results. In this study, deviations between measured and simulated moisture content were calculated

using the coefficient of determination in successive trials, as follows: equation(6) R2=1−∑(Xexp−Xcomp)2∑(Xexp−X¯exp)2 The Differential Evolution and Levenberg–Marquardt methods were implemented. Fluorouracil purchase Differential Evolution (DE) is an evolutionary algorithm proposed by Storn and Price (1995). Although DE shares similarities with other evolutionary algorithms (EA), it differs significantly in that the search process is guide based on information about the distance and direction of the current population. DE uses the differences between randomly selected vectors (individuals) as the source of random variations for a third vector (individual), referred to as the target vector. Trial solutions are generated by adding weighted difference vectors to the target vector. This process is referred to as the mutation operator in which the target vector is mutated. A crossover step is then applied to produce an offspring, which is only accepted if it improves the fitness of the parent individual. The basic DE algorithm is described in greater detail below with reference to the three evolution operators: mutation, crossover, and selection.

Intermediate oxidation states of chromium, i e Cr(V) and Cr(IV),

Intermediate oxidation states of chromium, i.e. Cr(V) and Cr(IV), are also proposed to play a role in chromium genotoxicity and carcinogenicity, either directly

or through reaction (e.g. via the Fenton reaction) with other Enzalutamide order cellular components, resulting in the generation of reactive oxygen species (see Fig. 4). It has been demonstrated that Cr(III) can be reduced to Cr(II) by the biological reductants, for example by l-cysteine and NAD(P)H, which in turn reacts with hydrogen peroxide via the Fenton reaction to produce hydroxyl radicals, detected by both Electron Paramagnetic Resonance spectroscopy and HPLC (Shi et al., 1993a and Shi et al., 1993b). Cr(III) species have been found to be capable of producing reactive oxygen species from both hydrogen peroxide and lipid peroxides. The formation of intermediate oxidation states of chromium, Cr(V) and Cr(IV) in both in vitro studies and in vivo animal studies administered Cr(VI) have been directly detected using EPR spectroscopy (Shi et al., 1993a and Shi et al., 1993b). In the course of the Cr(VI) reduction, many reactive oxygen species, including free radicals, such as the hydroxyl radical, singlet oxygen, superoxide see more anion are formed. Generated hydroxyl radicals are able to react with DNA

bases, e.g. guanine producing a variety of radical adducts, the best described is 8-hydroxyguanosine (8-OH-dG), a good marker of oxidative damage of an organism. Several types of DNA damage occur in chromium(VI)-exposed cells, including single-strand breaks, DNA–DNA interstrand crosslinks, DNA–protein crosslinks, chromium–DNA adducts, oxidative nucleotide

changes and chromosomal aberrations (De Flora and Wetterhahn, 1989 and Singh et al., 1998). Chromium is known to activate the MAP kinase signal transduction pathway. NF-κB, ATF-2 and p53 participate in regulation of critical cellular processes, including click here apoptosis. Cr(VI)-induced oxidative stress triggers the hypoxia signalling pathways, leading to increase in HIF-1α and VEGF protein levels. Chromium(III) deficiency in humans has been associated with cardiovascular disease, metabolic disease (e.g. diabetes) and infertility (see below). Chromium(VI) at high doses is considered to be the greatest health risk (Keegan et al., 2008). Cr(VI) enters the body by all three of routes of exposure: inhalation, ingestion or absorption through the skin. For occupational exposure, the airways and skin are the primary routes of uptake (De Flora et al., 1995). Breathing high levels of chromium(VI) can cause irritation to the nasal cavity, breathing difficulty (asthma and cough). Skin contact with certain chromium(VI) compounds can cause skin ulcers. Allergic symptoms such as redness and swelling of the skin have been reported following contacts with chromium compounds.

In fact, it has been demonstrated that the saturated FA are poten

In fact, it has been demonstrated that the saturated FA are potent inducers of activation of the transcription factor NF-κB, through its connection with the Toll like receptor 4 (TLR4) ( Lee et al., 2004). When the FA binds to the receptor TLR4, there is an immediate activation of intracellular pathway leading to NF-κB activation and increased gene transcription of iNOS selleck compound with subsequent increase in NO production. In FA-treated cells with BSA, there was a total inhibition of NO production. Therefore, we can assume that the increase of NO production induced by the mixture of FA could be due to activation of NF-κB and increased iNOS expression by direct

activation of TLR4. It was recently shown by our group that ASTA also increases the production of NO in human lymphocytes and neutrophils ( Bolin et al., 2010 and Macedo et al., 2010). As previously shown, ASTA was able to reduce the arterial blood pressure mediated by increase of NO production ( Hussein et al., 2005). However, ASTA reduced the activation the transcription factor NF-κB and decreased the IL-6 production in microglial cells ( Kim et al., 2010). In the current study, ASTA led to an increase in NO production and association of ASTA and FA-treated cells was not able to restore the NO

production ( Fig 3D). Therefore, we can suggest the ROS participation on NO induction, since a slight reduction on ROS production promoted by ASTA also promoted a small reduction in NO levels on FA + ASTA group. In

fact, NAC treatment partially reduced the production of NO induced LDK378 datasheet by FA, indicating a partial contribution of ROS in the NO production by FA. Contrasting results were obtained by Choi et al. (2008) which showed astaxanthin inhibiting the production of inflammatory mediators by blocking iNOS and COX-2 activation or by the suppression of iNOS and COX-2 degradation. Then, as in our FA mixture there is a great content of saturated FA and this FA can induce both the activation of TLR4 pathway which in turn activates nuclear transcriptor factor NFκB by different ways as previously described very by other authors ( Lee et al., 2004), we can assume there is the activation of TLR4-pathway, with a consequent induction of NFκB, followed by iNOS activation, which culminates in increased NO levels. ASTA was unable to abrogate the NO producing induced by the FA mixture. Excessive levels of reactive oxygen species not only directly damage cells by oxidizing DNA, protein and lipids, but indirectly damage cells by activating a variety of stress-sensitive intracellular signaling pathways such as NF-κB, p38 MAPK, JNK/SAPK, hexosamine and others. Activation of these pathways results in the increased expression of numerous gene products that may cause cellular damage and play a major role in the etiology of the late complications of diabetes (Newsholme et al., 2007).

It should also be noted that an internalization of clustered rece

It should also be noted that an internalization of clustered receptors will depend on the cytoskeleton and thus also on plasma membrane remodeling. Concerning TNF receptor Selumetinib concentration 1 (TNFR1), it has been reported that lipid rafts could promote the formation of a multi protein complex containing RIP, TRADD and TRAF-2 (Legler et al., 2003). This TNFR1-related complex may inhibit apoptosis through an activation of NF-κB (Muppidi et al., 2004). Recently, it has been described that ursodeoxycholic acid induced apoptosis via TRAIL-R2/DR5 localization in lipid rafts ( Lim et al., 2011). Although less systematically

investigated, changes in plasma membrane may also be involved in intrinsic apoptosis. Plasma membrane has been reported to play a role in the intrinsic apoptosis induced by arsenic (Hossain et al., 2000) oxysterols (Berthier et al., 2004) or B[a]P (Gorria et al., 2006, Tekpli et al., 2010a and Tekpli et al., 2010b). More specifically, lipid rafts appear to regulate the JNK activation related to Ruxolitinib solubility dmso arsenic-induced apoptosis

in T-cells (Hossain et al., 2000). We have also recently found that plasma membrane remodeling was involved in the B[a]P-induced intrinsic apoptosis in several cell types (Gorria et al., 2006, Tekpli et al., 2010a and Tekpli et al., 2010b). B[a]P-induced plasma membrane remodeling may result in alterations in intracellular pH homeostasis by acting on Na+/H+ exchanger 1 (NHE-1) and/or on intercellular communication (Tekpli et al., 2010b and Tekpli et al., 2012), processes further involved in the intrinsic apoptotic cascade. Interestingly, changes in the NHE-1 sub-membrane localization due to plasma membrane remodeling seems to be important for its activity (Tekpli et al., 2008 and Tekpli et al., 2012). By regulating this exchanger activity, plasma membrane remodeling appeared N-acetylglucosamine-1-phosphate transferase to be involved in B[a]P-induced intrinsic apoptosis, notably via a relocation of hexokinase II from mitochondria to cytosol ( Dendele et al., 2012 and Huc et al., 2007). Fig. 2 schematizes the detailed intracellular signaling pathway involved in

B[a]P-induced plasma membrane remodeling and apoptosis in the rat epithelial cell line F258. Intracellular pH caused by an activation of NHE1 has also been reported to regulate the activity of Bax ( Tafani et al., 2002), or possibly even more directly control caspase activities ( Lagadic-Gossmann et al., 2004). Interestingly, plasma membrane remodeling might also regulate intracellular calcium during apoptosis ( Berthier et al., 2004 and Takahashi et al., 2006), thereby affecting the function of Bcl-2 family members like Bad. In mouse hepatoma Hepa1c1c7 cells, we have found that B[a]P increases gap junctional intercellular communication via a change in localization of connexin 43 from Golgi apparatus and lipid rafts, to form gap junction plaques at the plasma membrane.

1–3 5 pg/mL) and demonstrate an increased concentration of endoge

1–3.5 pg/mL) and demonstrate an increased concentration of endogenous cytokines in disease, which were in keeping with mRNA expression data. These findings are consistent with published data on relative protein levels of these cytokines in Hp-infected and uninfected patients measured by ELISA, western blotting and Luminex in supernatants from gastric biopsy homogenate or gastric biopsy culture ( Bodger et al., 1997, Luzza et al., 2000, Shimizu et al., 2004, Mizuno et al., 2005 and Serelli-Lee et al., 2012). Sensitive measurement of cytokine ERK inhibitor profiles using methodology that better reflects in vivo

concentrations is technically challenging. Optimisation of processing methods can improve data acquisition from precious tissue samples. A number of factors need to be considered when selecting an assay, including the type and quantity of samples, the availability and multiplexing capabilities of the desired analytes, the expected range of concentrations and sensitivity required, specificity, accuracy, precision, time and cost. We selected Luminex assays from MILLIPLEX for use in future studies based on our evaluation findings. Together with our optimised sample preparation protocol we concluded that Luminex assays are a suitable

technique for quantifying endogenous cytokines in mucosal biopsies. We hope that our approach will be more widely relevant for those seeking to quantify multiple cytokines in small tissue samples. The authors thank Dr Ian Spendlove, Dr Ann Lowe and Prof Jan Bradley for use of their Bio-Plex 200 systems, Dr Maria Toledo-Rodriguez for use of her Gemcitabine cost TissueLyser LT, and the patients and staff at Nottingham University Forskolin Hospital. We purchased all kits

used in this study. The study design, collection, analysis and interpretation of data, writing of the report and decision to submit for publication were undertaken independently by the authors without involvement of the funders or kit manufacturers. ES and RI are supported by Clinical Research Training Fellowships from the Medical Research Council [grant numbers G0701377 and G1000311]. This article presents independent research supported by the National Institute for Health Research (NIHR), through the NIHR Biomedical Research Unit in Gastrointestinal and Liver Diseases at Nottingham University Hospitals NHS Trust and the University of Nottingham. The views expressed are those of the author(s) and not necessarily those of the NHS, the NIHR or the Department of Health. “
“Several groups have attempted with varying degrees of success to improve bacterial production of antibody fragments by co-expressing them with molecular chaperones or folding catalysts (Bothmann and Pluckthun, 1998, Strachan et al., 1999, Bothmann and Pluckthun, 2000, Levy et al., 2001, Mavrangelos et al., 2001 and Maynard et al., 2005). The correct folding of scFv and Fab antibody fragments is highly dependent on the activity of peptidyl prolyl cis-trans isomerases (PPIases).

The TFC system is based too strongly on market and economic consi

The TFC system is based too strongly on market and economic considerations and does not take into account social factors. In several EU countries, this has helped to rationalize the fleet (usually decreasing the number of vessels). But this type of economic speculations

would be detrimental for the Mediterranean Regions, which are characterized by a huge number of vessels (and fishermen) belonging to the artisanal small-scale fisheries. TFCs would also increase job entry barriers for new generations. In order to enter the profession, TFCs or licenses must be purchased, and this has a cost which is proportional to the potential incomes. Building or buying a fishing vessel in order to get a TFC is very expensive, usually too see more expensive compared to potential incomes, considering the current crisis of the sector. In addition one of the criticalities of TFCs is the concentration of TFCs in the hands of a few vessel owners (the risk for bigger fishing enterprises

to absorb smaller ones SB203580 is high) could cause an exit of small fishing vessels, thus making new entries to the profession even more difficult. All partners considered that the adoption of a TFC system would lead to a fleet reduction. Introducing new restrictions (quota and/or fishing days), the potential income for each enterprise is reduced. Some of the fishermen will therefore have to exit the sector because staying in is not remunerative anymore. It is however difficult to foresee TFC markets and prices. In certain cases

the monopoly can be obtained through a concentration of licenses rather than the organization of fishermen in Consortia or Producers’ Organizations. The best way to avoid excessive concentration would be to exclude small-scale fisheries, as well as species which do not have a quota. According to the MAREMED partners, throughout the Mediterranean fishermen and category associations are mainly worried about a potential TFC introduction. One of the reasons is related to what has happened with the introduction of quotas for tuna: this type of fisheries has almost disappeared Arachidonate 15-lipoxygenase as a consequence. Overall, actors and stakeholders in the fisheries sector have however not a clear vision of how a TFC system could actually work, since this issue is managed with a top-down approach, including the setting of quotas and fishing times. Fishermen of the small pelagic fisheries sector in the Adriatic Sea showed a direct interest in developing management schemes based on quotas directly managed by the fishermen themselves; however the recent GFCM (General Fisheries Commission for the Mediterranean) Recommendation [42] excluded fishermen and Member States from the definition of quotas and fishing period in the Adriatic Sea. The state of heavy exploitation of Mediterranean fishery resources is apparent, and for some stocks it has reached critical levels.

5 mg/mL) for 4 h at 37 °C in a 5% CO2 atmosphere

The pla

5 mg/mL) for 4 h at 37 °C in a 5% CO2 atmosphere.

The plate was centrifuged at 1500 rpm for 10 min. The medium was removed and replaced by 100 μL of dimethyl sulfoxide (DMSO), followed by mixing to dissolve the formazan this website crystals. Absorbance was measured at 570 nm on a microenzyme-linked immunosorbent assay (ELISA) reader (Spectramax, Molecular Devices®) and the reduction of cell viability was expressed as the percentage compared with the negative control group designated as 100%. A control experiment carried out using only PAMAM in the culture medium did not induced cytotoxicity (data not shown). Nanoparticle-induced DNA damage was performed by the comet assay (also referred to as the single-cell gel electrophoresis – SCGE analysis) under alkaline conditions (Singh et al., 1988). The negative control was

exposed without AuNps under the same conditions. HepG2 cells and PBMC were cultured in 12-well culture plates as described above, and then pretreated for 3 h with 1.0 and 50.0 μM of AuNps-citrate and AuNps-PAMAM. Microscope slides were prepared in duplicate and coated with 1% normal melting point agarose (NMA). 60 μL of each cell suspension with 300 μL of low melting point agarose 1% (LMPA) were placed on these microscope slides containing NMA, deposited over the agarose layer. Coverslips were placed on the gels, which were left to set on ice. After gently removing the coverslips, the slides were immediately submersed in cold lysis solution (2.5 M NaCl, 100 mM EDTA,

10 mM Tris, 1% Tritron Panobinostat Prostatic acid phosphatase X-100, pH 10) for 12 h in the dark. DNA was then allowed to unwind for 20 min in alkaline electrophoresis solution (300 mM NaOH, 1 mM EDTA, pH > 13). Electrophoresis was performed under 25 V and 300 mA for 20 min. Subsequently, the slides were placed in a cold neutralizing buffer (400 mM Tris buffer, pH 7.5) for 15 min, dried in 100% methanol for 5 min, and stained with 50 μL of 20 μg/mL ethidium bromide in the dark. At least 50 comets per slide were analyzed under a fluorescence microscope (Nikon Eclipse E200, Japan) equipped with an excitation filter of 515–560 nm and a barrier filter of 590 nm, connected to a digital camera (Nikon DS Qi1, Japan). The classical visual analysis scoring of the comet assay was analyzed by a single analyst, in order to minimize scoring images variation. Data were based on 150 cells for each test or control that were visually scored as belonging to one of five classes, according to tail size and intensity. Classes 0, 1, 2, 3, or 4 were given, with 0 = no detectable damage and 4 = maximum damage. The damage index was obtained by the formula, damage index = (0 × n0) + (1 × n1) + (2 × n2) + (3 × n3) + (4 × n4). The variables n0–n4 represent the number of nucleoids with 0–4 damage level, and each experiment was performed in triplicate. The AuNps cellular uptake was investigated using flow cytometry (Suzuki et al., 2007).

The salinity data from mid-water and bottom

depth at stat

The salinity data from mid-water and bottom

depth at station M5 and the surface salinity at station M3 were low-passed using the 34-h Lanczos filter to obtain the sub-tidal record. As for other datasets, the Chesapeake Bay National Estuarine Research Reserve (CBNERR) measured surface salinity at two stations, Taskinas Creek and Clay Bank in the York River (YR), VA. During Hurricane Isabel, salinity was measured by YSI-6600 Sondes operated by CBNERR at fixed stations at Sweet Hall, Taskinas Creek, Clay Bank, and Goodwin Islands in the YR. Meteorological data were collected from a total of 13 stations around CB operated selleck chemical by NOAA and the National Data Buoy Center (NDBC). Typically, wind data were taken at a height of 10 m above mean sea level (MSL) and atmospheric pressures were observed at MSL. River stream flow data from CB tributaries were obtained from the US Geological Survey (USGS) for both hurricanes (Table 3). The baroclinic circulation in CB was

performed using the semi-implicit Eulerian–Lagrangian Finite Element (SELFE) model, a free surface hydrostatic, three-dimensional VX-809 supplier cross-scale circulation model on unstructured grids (Zhang and Baptista, 2008, Liu et al., 2008a, Liu et al., 2008b and Burla et al., 2010). SELFE uses a semi-implicit Galerkin finite-element method for the pressure gradient and the vertical viscosity terms, which are treated implicitly, and for other terms treated explicitly. To solve the vertical velocity, a finite-volume method is applied to a typical prism, because it serves as a diagnostic variable for local volume conservation when a steep slope is present (Zhang et al., 2004). SELFE treats the advection in

the transport equations with the total variation diminishing (TVD) scheme. A higher-order finite-volume TVD scheme is a preferable option in SELFE. TVD is the technique of obtaining high-resolution, second-order, oscillation-free, explicit scalar difference Vildagliptin schemes by the addition of a limited anti-diffusive flux to a first-order scheme (Sweby, 1984). Osher (1984) defined the flux differences for a general three-point E-scheme, which is a class of semi-discrete schemes approximating the scalar conservation law. These flux differences are used to define a series of local Courant–Friedrichs–Levy (CFL) numbers. Superbee (Roe, 1986) is used as a flux limiting function. SELFE adapts the Generic Length Scale (GLS) turbulence closure through the General Ocean Turbulence Model (GOTM) suggested by Umlauf and Burchard, 2003 and Umlauf and Burchard, 2005, taking advantages from a number of level 2.5 closure schemes such as k–ε ( Rodi, 1984), k–ω ( Wilcox, 1998); Mellor and Yamada scheme ( Mellor and Yamada, 1982). In this study, the k–ε scheme is used. The horizontal grid used is shown in Fig. 3. This grid has 20,784 elements, 11,582 nodes, and 32,386 sides on the surface. At least three horizontal grid cells resolve the channel of the main Bay.