Our final objective is to identify the specific geographic locations(s) in the TNMPA, if any, that were preferentially and recurrently used by belugas during the July aggregation period, and by doing Veliparib so, provide a tool that could be used by regulators for assessing developments, setting terms and conditions for activities

that are proposed by industry, and evaluating changes in the location of preferred areas. The results we present are timely given recent renewed interest by the hydrocarbon industry in the Beaufort/Mackenzie region (AANDC, 2012) and Canada’s legal requirement to design and undertake monitoring programs in the TNMPA (Loseto et al., 2010, Canada Gazette, 2010 and Beaufort Sea Partnership, 2014). In addition, knowledge of beluga critical habitats and the ways in which they have used them in the past may also help us in the future to predict how belugas have or will respond to climate change or other factors that alter habitat (Laidre et al., 2008). Systematic aerial surveys were conducted over six summers between late June and early August, 1977–1985, and in late July 1992, to monitor the distribution and relative abundance of belugas in all four bays (subareas) of the Mackenzie Estuary (Niaqunnaq Bay, East Mackenzie Bay,

West Mackenzie Bay and Kugmallit Bay), including portions of the estuary that would eventually become the TNMPA in 2010. A total of 169 subarea surveys were attempted or completed during this period. The same

systematic transect lines were flown in all survey years in the 1970s and 1980s (Fig. 2), with transects spaced at intervals of 3.2 km, except in West Mackenzie Bay where they were spaced at 4.8 km. GSK2118436 A strip-transect method was used (Caughley, 1977) in all surveys, with a strip width of 1.6 km (800 m per side), except in Low-density-lipoprotein receptor kinase 1992 when the strip width was 400 m per side (Harwood et al., 1996). This provided survey coverage of 50% in the 1970s and 1980s (33% in West Mackenzie), and 29% and 15% in July 1992, respectively. Survey altitude was 305 m during all surveys, which was measured with the aircraft’s altimeter, and adjusted by the pilots during the surveys as necessary. Target ground speed was 200 km/h. Sighting coordinates were calculated using ArcGIS, using start and end-coordinates for each transect, and elapsed time. Mean ground speed for all surveys pooled was 188 km/h (SD 54.2). Primary search positions were equipped with bubble windows in 1984, 1985 and 1992, for enhanced visibility under the aircraft, close to the flight path. Surveys were flown in Cessna 185 on wheels (1970s) and in de Havilland Twin Otters (1980s and 1992). Survey conditions were assessed and recorded by observers at the beginning and end of each transect, and were summarized in the database for each subarea survey, by transect line. The usual flying time was 6–8 h per day. Observers rested during ferrying flights, refuelling stops, and when flying between transects.

In addition, our data suggests that pentamidine could actually improve the delivery of nifurtimox, which is in line with previous work by our group in an animal model. Nifurtimox (MW 287.30) was custom labelled with

tritium (3H 3,4 furam ring) specific activity: 2 Ci/mmol) by Moravek Biochemicals (California, USA). [14C]sucrose (4980 mCi/mmol) was purchased from Moravek Biochemicals. Unlabelled suramin, eflornithine and pentamidine isethionate sodium salt were purchased from Sigma Chemical Company (Dorset, UK). Unlabelled nifurtimox and melarsoprol were a kind gift from Professor S. Croft (London http://www.selleckchem.com/products/Y-27632.html School of Hygiene and Tropical Medicine, UK). Probenecid, indomethacin and dimethyl sulfoxide (DMSO) were purchased from Sigma Chemical Company. Dexamethasone and Pheophorbide A (PhA) were purchased from Acros Organics, (Fisher Scientific, Loughborough, UK). Para-aminohippuric acid (PAH) and taurocholic acid (TCA) were purchased from MP Biochemicals, UK. Ko143 and haloperidol were purchased from Tocris Bioscience (Bristol, UK) and Sigma, respectively. The hCMEC/D3 cell line was obtained from Professor Pierre O. Couraud (Institut Cochin, Université Paris Descartes, CNRS, Paris, France) and Dr Ignacio Romero (The Open University, Department of Life Sciences, Walton Hall, Milton Keynes, UK). The EGM-2MV BulletKit was purchased from Lonza (Basel, Switzerland). All cultureware was Nunclon brand

and purchased from Thermo Scientific, UK. Rat tail collagen 1 and penicillin-streptomycin were purchased from Gibco, Invitrogen, Urease (Paisley, UK). HEPES 1M was purchased from R428 in vivo Sigma Chemical Company. Primary mouse anti-P-gp/MDR1 [C219] (ab3364), anti-BCRP/ABCG2

[BXP-21] (ab3380) and mouse anti-GAPDH monoclonal antibodies [6C5] (ab8245), rabbit polyclonal secondary antibody (HRP) (ab6728) were purchased from Abcam, Cambridge, UK. Goat anti-rabbit Alexa Fluor 488 was purchased from Invitrogen, UK. HepG2 cells were a kind gift from Mr Enrico Cristante (Imperial College London, UK). Rabbit anti-human von Williebrand factor (vWF) (P0226, Dako, Stockport, UK) was a kind gift from Dr Sarah Chapple (King’s College London). The hCMEC/D3s were cultured in EBM-2 endothelial growth medium supplemented with HEPES, penicillin–streptomycin, 2.5% foetal bovine serum (FBS), insulin-like growth factor-1, vascular endothelial growth factor, epidermal growth factor, hydrocortisone and basic fibroblast growth factor from the EGM-2MV BulletKit as previously described (Poller et al., 2008). All cells used in the experiments were seeded at a density of 2.5 × 104 cells/cm2 and were between passages 28 and 35. Before seeding, cells were checked for viability by 0.4% Trypan Blue solution in a haemocytometer. Cultureware was coated with 0.1 mg/ml rat tail collagen type 1 for 2 h at 37 °C prior to seeding. Cells were cultured in an incubator with a saturated humidity at 37 °C in 5% CO2 and 95% fresh air and grown to 80–90% confluency before seeding (after 3 days).

The distance δi(x0, y0, z0) of the ith trajectory from the point (x0, y0, z0) is calculated for a given set of trajectories. The trajectories for which δi(x0, y0, z0) is larger than kds(x0, y0, z0) are discarded, where k is a fixed

parameter. This leaves a subset S1 of events and a new (smaller) mean deviation ds1(x1, y1, z1), from which an improved location (x1, y1, z1) of the strongest tracer is calculated. The algorithm proceeds until only a specified fraction f of the initial trajectories remains, i.e. terminates at step n, where N(Sn) = fN(S). The parameter k determines the rate at which trajectories are discarded. Values of k between 1 and 1.5 have been investigated. The optimum lies somewhere between these two extremes Selleck CB-839 GW-572016 ( Parker et al., 1993). If the parameters

f1, f2 and f3 are defined as the first-, second- and third-tracer fractions of the initial trajectories respectively and another parameter ρ as the fraction of the desired trajectories in the entire original set S, the specified fraction f of the initial trajectories is equal to ρf1 for the first strongest tracer. The parameter ρ has been investigated, and its optimum value lies between 0.20 and 0.33 ( Parker et al., 1993). After the strongest tracer is located, trajectories passing close to the located tracer are then removed from the dataset. In a similar way, repeating the above those procedure, the locations of the second and the third tracers are then calculated. And then the amount of γ-rays is recalculated around each located tracer for the entire

original set S of trajectories to make sure the first, second and third highest amount of γ-rays around the tracers correspond to the first, second and third strongest tracers respectively. The final outcome is that the subsets SF1, SF2 and SF3 of trajectories are selected from the original set, from which the locations of tracers 1, 2 and 3 are calculated as their minimum distance points (xF1, yF1, zF1), (xF2, yF2, zF2) and (xF3, yF3, zF3) respectively during the time interval covered by these subsets. Each event Li has its time of measurement ti recorded, and the location thus arrived at is considered to represent the tracers’ position at time equation(4) t=1NF∑SFtiwhere NF ≡ N(SF) is the number of trajectories in the final subset, and SF = SF1 ∪ SF2 ∪ SF3. Having located the tracers once, the new set starts immediately after trajectories have been discarded in the previous set. Translational and rotational motions of any regular shape solid can be reconstructed by tracking three tracer particles if the positions of the particle are well designed. This paper uses cubed potato as an example to demonstrate the reconstructions.

These hydrolases are normally confined at high concentrations in cytoplasmic vesicles (granules) and only released upon cell activation. Detergents can easily free the proteases from the granules. It was shown that even the presence of one PMN per million RBCs is able to release enough proteolytic power to damage, if not fully inhibited, highly sensitive RBC proteins such as ankyrin

and protein 4.1.6 Enzalutamide in vivo Another common situation that could give rise to artefactual results is the preparation of “ghosts” from RBCs by hypotonic haemolysis.17 If the RBCs are contaminated by PMNs and the buffers used are not effectively supplemented with anti-proteases, the RBC membrane proteins will almost certainly be damaged (Fig. 1B, C). The workaround to this problem is the filtration of the blood and the use of freshly prepared lysing buffers containing a working concentration of anti-proteases. Other factors that must be standardised to be able to compare the obtained data between different laboratories are the temperature, shear stress, medium content, especially traces of serum, and the condition of cells used in the experiments. Furthermore, recent studies emphasise the importance of co-factors and substrates of several receptors, which may contribute to the experimental outcome. Temperature-related artefacts include ion misbalance and the ensuing changes in cell volume and Ca2 +-dependent

processes. Temperature Anticancer Compound Library manufacturer sensitivity depends on the particular approach, but it can be severe, differing, e.g., between different types of ion transporters. The decrease in the activity of ion transporters with a decrease in temperature by 10° (Q10) is approximately

30-fold for the PAK5 Ca2 + pump,18 approximately 3-fold for the Na+/K+ pump19 and approximately 1.5–3-fold for most of the ion transporter systems.[20] and [21] Thus, temperature changes may have a pronounced effect on the intracellular Ca2 + levels and the Na+/K+ distribution. The temperature may not necessarily be fixed at 37 °C in particular experimental settings (e.g., controlling the temperature can be complicate for patch-clamp investigations). However, temperature as a factor has to be taken into account, and the potential side effects must be controlled. Serum and the multiple biologically active factors it contains, including albumin and factors bound to it, such as interleukins, prostaglandins, insulin and amino acids, can introduce artefacts. Depending on the experimental settings, investigations are conducted in serum-containing or serum-free media. Proteins introduced with serum have been shown to play an active role in regulating the activity of ion transporters in RBCs obtained from healthy and diseased subjects. Little is known about the serum components mediating the effects. It has been shown that lysophosphatidic acid (LPA) activates Ca2 + uptake by RBCs.

Improved monitoring and analytical methods draw attention to unknown and invasive organisms and raised awareness of existing risks. Examples along the southern Baltic coast are recently observed high concentrations of native vibrions (Vibrio vulnificus), which caused lethal infections in the coastal Baltic Sea and are today considered as a major threat for summer seaside resorts in Germany ( Böer et al., 2010). Another example of a new challenge is Escherichia coli O157:H7, an E. coli strain that can produce toxins and can cause gastroenteritis, urinary tract infections PLX4032 purchase and neonatal meningitis (e.g. Mudgett et al., 1998 and Paunio

et al., 1999). Many other, potentially more problematic microorganisms, might EPZ-6438 manufacturer create problems in our coastal waters ( Roijackers and Lürling, 2007). Even if bathing water meets the microbiological standards of the European Bathing Water Directive (2006/7/EC), many potential pathogenic organisms could be present ( WHO, 2009). Furthermore, many of these microorganisms will benefit from climate change and might cause increasing problems in future. Against this background, new simulation, management and decision support tools for bathing water quality are required. We present a new on-line bathing water quality information system. The system has been developed within

the project GENESIS as a general European approach to support regional authorities. It combines a model and simulation tool with an alerting and improved communication system. The model tool consists of a three-dimensional flow model (GETM) together with a Lagrangian particle tracking routine (GITM). Here, we exemplary apply our model tool and prove its suitability as well as its potential and practical relevance. Spatially, we focus on the Szczecin Parvulin lagoon at the German/Polish border (southern

Baltic coast). The Lagoon is affected by the Odra river and sewage water of Szczecin city and is a pollution hot-spot region. Insufficient bathing water quality causes beach closures and hampers tourism development. In several scenario-simulations we give an overview how climate change might affect the survival of various human-pathogenic organisms in this region and assess how the spatial contamination risk in the lagoon will alter in future and show the benefit of the bathing water quality information system. In these scenarios we focus on the indicators of the European Bathing Water Directive (2006/7/EC), namely enterococci and E. coli bacteria. The Odra (German: Oder) coastal region, with the large Szczecin lagoon, is located at the German and Polish border in the southern Baltic. The lagoon covers an area of 687 km2 and has an average depth of 3.8 m. Tourism is the major source of income in the coastal region.

Preparation of freeze-dried broccoli has been optimized to preserve glucosinolates and prevent inactivation of myrosinase. This is particularly important because SFN is not stable and is more bioactive when fed to rats in its glucosinolate precursor form than when hydrolyzed before being fed to rodents [34]. Addition of 10% to 20% freeze-dried broccoli to rodent diet has been reported

to increase activity of hepatic and colonic ARE enzymes [58], [59] and [60]. In contrast to these reports, 10% broccoli diet used in our studies did not increase ARE genes in brain or liver tissue of aged mice. However, in this study, HMOX1 was induced by LPS, suggesting that this gene is activated in response to increased oxidative stress generated by LPS-induced inflammation [61]. Heme oxygenase I is an endogenous antioxidant that inhibits inducible nitric oxide synthase in LPS-stimulated macrophages, Selleckchem UK-371804 and higher HMOX1 mRNA and protein are associated with an anti-inflammatory macrophage phenotype [62], [63] and [64]. Although HMOX1 is notable as part of the antioxidant cascade activated by Nrf2, HMOX1 mRNA expression was also responsive to inflammation induced by LPS. Induction of HMOX1 by LPS in our model was an expected component in agreement with findings MS-275 solubility dmso indicating that, in addition to containing an Nrf2-inducible ARE promoter region,

HMOX1 is up-regulated

by the proinflammatory NFκB transcriptional pathway that is strongly activated by LPS [65]. On the basis of our findings, HMOX1 appears to be more transcriptionally responsive to activation of NFκB during inflammation than to 10% broccoli diet. A 10% broccoli diet may be insufficient to elevate SFN levels in circulation to temper acute inflammation in mice. In agreement with this suggestion, Innamorato et al [36] reported that HMOX1 protein is induced in the brain by a high dose of SFN injected intraperitoneally, but there are no published data reporting in vivo induction of HMOX1 transcription and translation after low doses of SFN such as that obtained when consuming broccoli-supplemented diet. A clinical study that examined gene expression in gastric these mucosa after consumption of broccoli soup reported that although several antioxidant genes were elevated in gastric mucosa, only a fraction of genes previously induced by SFN in vitro were altered by the broccoli soup [66]. It is evident that additional preclinical and clinical studies are needed to determine effective timing and dosage of broccoli inclusion in the diet. Another explanation for the lack of ARE gene expression induced by broccoli diet is that other peripheral tissues, such as intestine or resident macrophages of the peritoneum, may be more sensitive to broccoli-supplemented diet.

Samples were obtained with informed consent. A detailed protocol Selleck FG 4592 for gastric culture is provided in the Supplementary materials. Briefly, glands were extracted from 1 cm2 of human tissue using EDTA in cold chelation buffer,17 seeded in Matrigel (BD Biosciences), and overlaid with medium containing advanced Dulbecco’s modified Eagle medium (DMEM)/F12 supplemented with penicillin/streptomycin, 10 mmol/L HEPES, GlutaMAX, 1 × B27 (all

from Invitrogen), and 1 mmol/L N-acetylcysteine (Sigma-Aldrich). Growth factors were added to the basal medium as indicated in the Figures. The final human stomach culture medium contained the following essential components: 50 ng/mL epidermal growth factor (EGF) (Invitrogen), 10% noggin-conditioned medium, 10% R-spondin1–conditioned medium, 50% Wnt-conditioned medium, 200 ng/mL fibroblast growth factor (FGF)10

(Peprotech), 1 nmol/L gastrin (Tocris), and 2 μmol/L transforming growth factor (TGF)βi (A-83-01; Tocris). The facultative component was 10 mmol/L nicotinamide (Sigma-Aldrich). After seeding, 10 μmol/L RHOKi (Y-27632; Sigma-Aldrich) was added. Additional tested components were as follows: 100 ng/mL insulin-like growth factor (IGF) (Peprotech), 10 μmol/L p38 inhibitor (SB202190; Sigma-Aldrich), 3 μmol/L GSK3β inhibitor (CHIR99021; Axon Medchem), and 500 nmol/L prostaglandin E (PGE)2 (Tocris). Approximately 1 cm2 of cancer tissue was cut into small fragments and washed in cold chelation buffer until the supernatant was clear. Fragments were subjected to enzymatic Baf-A1 mw digestion by 1.5 mg/mL collagenase (Gibco) and Lumacaftor manufacturer 20 μg/mL hyaluronidase (Sigma) in 10 mL advanced

DMEM/F12 (Gibco), supplemented with antibiotics (Primocin; Invivogen), for 1 hour at 37°C with shaking. Cells were washed twice in advanced DMEM/F12, seeded into Matrigel, and overlayed with medium containing HEPES, GlutaMAX, penicillin, streptomycin, B27, n-acetylcysteine, EGF, R-spondin1, noggin, Wnt, FGF10, gastrin, TGFβ inhibitor, and RHOK inhibitor as described earlier. Bacterial strains and culture conditions are specified in the Supplementary materials. For infection studies, organoids were seeded in 50 μL Matrigel in 4-well multidishes (Thermo Scientific). Antibiotic-free medium was refreshed every 2–3 days, with a minimum of 3 medium changes before infection to allow removal of antibiotics from the culture. Organoids were microinjected on day 10 after seeding with an approximate multiplicity of infection (MOI) of 50 unless otherwise stated. For calculation of MOI, organoids were disrupted into single cells by EDTA and cells were counted (approximately 4000 cells/organoid). To achieve a final MOI of 50, bacteria were suspended in advanced DMEM/F12 at a density of 1 × 109/mL and organoids were injected with approximately 0.2 μL bacterial suspension using a micromanipulator and microinjector (M-152 and IM-5B; Narishige) under a stereomicroscope (MZ75; Leica) inside a sterile bench (CleanAir).

Riegl (1995) found surge-induced peak suspended-sediment concentrations of up to 389 mg L−1 in sandy gullies and 112 mg L−1 over coral on South African reefs; this, however, was local sediment stirred up and immediately re-deposited. While the studies above demonstrate that coral reefs and turbidity/sedimentation can coexist, it also shows the danger of introducing sediment since it is likely to be remobilised repeatedly.

All the reef systems discussed in the previous two paragraphs were clearly adapted to sedimentation and turbidity, with mostly low accretion rates demonstrated in South Africa (Ramsay and Mason, 1990 and Riegl et al., 1995) and quite high accretion rates on inshore reefs from the Great Barrier Reef (Larcombe selleck inhibitor et al., 1995), comparable to those in “optimal” environments. Corals that are naturally exposed to high and variable background conditions of turbidity and sedimentation (e.g. due to storms and/or river influence) will show higher tolerances to short increases in turbidity or sedimentation PD-0332991 clinical trial caused by dredging (Nieuwaal, 2001). Corals from shallow-water environments, where they are frequently exposed to elevated temperatures,

storms and wave action, are more likely to be tolerant of environmental stresses than corals in deeper waters (Brown and Howard, 1985, Hoeksema, 1991b and Hoeksema and Matthews, 2011). A synthesis of literature data regarding the sensitivity of different coral species to turbidity is presented in Table 5. These data were reworked and related to a relative sensitivity index according

to the response matrix presented in Table 6. Sensitivity classes were then given scores from 1 to 5, with 1 corresponding to “very tolerant” and 5 to “very sensitive”. The scores for individual coral species were subsequently related to their dominant growth form and mean Etofibrate calyx diameter. Analysis of these data (90 entries for 46 species) confirmed that there is a significant relationship (Kruskal–Wallis, P < 0.05) between the growth form of corals and their sensitivity to turbidity ( Fig. 5a). Most soft corals and many massive coral species are relatively sensitive to turbidity while laminar, plating and tabular corals as well as some morphologically variable corals are relatively tolerant. There was no significant relationship between the calyx diameter of corals and their sensitivity to turbidity ( Fig. 5b). Most coral species are sensitive to enhanced sedimentation, even in the order of a few centimetres per year (Rogers, 1990). Pastorok and Bilyard (1985) suggested that sedimentation rates of >50 mg cm−2 d−1 (equivalent to 500 g m−2 d−1) may be considered catastrophic for some coral communities, while 10–50 mg cm−2 d−1 could be classified as moderate to severe.

Clopidogrel

belongs to the anti-P2Y12 thienopyridine family, which are pro-drugs metabolized into an active compound see more by several P-450 cytochromes (CYP450) in the liver. It acts on the ADP receptor P2Y12 (Fig. 2), by covalent modifications of two cysteine residues. The P2Y12 receptor is important for the amplification of the platelet activation process, not only when platelets are stimulated with ADP, but also with other agonists such as collagen [5]; it also plays a major role in thrombus formation in high shear stress conditions [21]. At the maintenance dose of 75 mg/day, maximal pharmacodynamic effect is reached between days 5 and 7 [22]. This delay between drug intake and antiplatelet effect can be partially overcome by the administration of an initial loading dose (600 mg). Patients at high risk of ischemic event (for instance after an acute coronary syndrome and/or percutaneous coronary intervention) are usually treated by using a dual anti-platelet therapy with aspirin and an anti-P2Y12 drug for between 1 and 12 months. Although it combines the advantages of both drugs, the efficacy of this treatment may be limited by compensatory platelet activation pathways partially restoring platelet reactivity [18]. Contrary to acute

settings, the dual antiplatelet therapy is generally not recommended in stable cardiovascular Morin Hydrate I BET 762 patients [22]. The delay and the variability of the pharmacodynamic effect of clopidogrel promoted the development of more efficient anti-P2Y12 drugs, such as prasugrel, a third generation thienopyridine drug, and ticagrelor, a non-thienopyridine molecule. Other platelet receptors or pathways are targeted

by antiplatelet drugs. Integrin αIIbβ3, for instance, is antagonized by several compounds (eptifibatide, abciximab or tirofiban), which are administered intravenously (Fig. 2). These treatments are often prescribed to patients in acute clinical situations [18] and [22]. Phosphodiesterase inhibitors, such as cilostazol and dipyridamole, increase levels of cyclic adenosine monophosphate, inhibiting platelet activation (Fig. 2) [22]. These latter drugs have specific side effects that limit their use in daily practice. Other antiplatelet drugs with new targets, such as the thrombin receptor PAR-1 or the collagen receptor GPVI, are in development [23] and [24]. Biological evaluation of platelet reactivity in CV patients treated with antiplatelet drugs shows that the efficacy of the drugs can vary between patients and that a significant proportion of treated patients are deemed “non-responders”, “poor responders” or “resistant”. This is because their platelet reactivity is higher and can even reach a level similar to that of patients without antiplatelet drug treatment [25].

The numerical oscillations visible in the Fluidity output become negligible at 1000 m resolution, with little difference between results at resolutions between 1000 m and 125 m buy Ceritinib ( Fig. 2). The observed numerical oscillations are caused by the sharpness of the leading and trailing edges of the slide, where minimal smoothing of 1000 m was used ( Haugen et al., 2005). Increasing

the smoothness of these edges (by increasing S in (9)) removes the oscillations. Clearly, the mesh resolution must be high enough to capture the smoothing length or the slide will have an effective flat front. To check that this was the cause of the spurious oscillations, the 5000 m resolution case was re-run with a smoothing length of 7500 m. The results show much reduced oscillations, but with the

wave form shifted due to the new location of maximum height ( Fig. 2). This experiment confirms the correct implementation of the boundary condition and shows how the assumed shape of the slide dictates the mesh resolution required in the slide area. A slide with steeper leading and trailing edges requires higher spatial resolution to eliminate numerical oscillations. To extend our validation PI3K Inhibitor Library in vivo of Fluidity’s new slide-tsunami model to three dimensions, we also replicated a simulation of landslide generated waves that are only weakly dispersive (Ma et al., 2013). Recent work by Ma et al. (2013) simulated the wave train produced by a rigid-block model in a three-dimensional domain on a constant slope. We can therefore compare Fluidity to the results shown in Ma et al. (2013). The domain is 8 ×× 8 km, with a constant slope of 4°. We set the minimum depth to be 12 m and the maximum to be 400 m. We used a horizontal model resolution

was 25 m in x   and y   and explored the influence of vertical resolution by performing simulations with 1–4 layers. Ma et al. (2013) use a different slide geometry to that described above, based on the work of Enet and Grilli (2007). The slide geometry is given by: equation(13) hs=hmax1-∊1coshkbx1coshkwy-∊where kb=2C/b,kw=2C/wkb=2C/b,kw=2C/w and C=acosh(1/∊)C=acosh(1/∊). The slide has length b=686b=686 m, width w=343w=343 m and thickness hmax=24hmax=24 Flucloronide m. The truncation parameter, ∊∊ is 0.717. The slides moves according to: equation(14) s(t)=s0lncoshtt0where s0=ut2/a0,t0=uta0,a0=0.27 m s−2, and ut=21.09ut=21.09 m s−1 as detailed in Ma et al. (2013). We use these definitions of the slide height and speed for comparisons to Ma et al. (2013). The resulting wave is very similar in magnitude and waveform to that shown in Ma et al. (2013), even using only a single layer in the vertical (Fig. 3). Convergence of the Fluidity model results is observed for three or more element layers (c.f. 40 layers used by Ma et al. (2013)), indicating that the wave is only weakly dispersive. In more detail, Fluidity produces slightly lower amplitude waves than those reported by Ma et al. (2013) (Fig.