miRNAs target complementary sequences in the 3′ untranslated region of specific mRNAs. As a result, target gene expression is repressed due either to translational inhibition and/or to mRNA degradation (reviewed

in Cannell et al., 2008, Fabian et al., 2010 and Jackson and Standart, 2007). Therefore, a small change in miRNA expression can have a profound effect on outcome making them an appealing area of research for the discovery of new mechanisms of action. The lack of hepatic miRNA response to BaP exposure as reported in Yauk et al. (2010) may be explained by: (1) few or no hepatic miRNAs under the transcriptional control of AHR or immediately responsive to DNA damage or (2) a high level of liver miRNA stability and lack of susceptibility to perturbation by BaP. Moreover, BaP exposure in rodents does not lead to liver cancer, but does cause cancer

in other tissues. Thus, we proposed that future experiments PLX4032 in vitro should investigate early miRNA response in a tissue that is susceptible to cancer development following BaP exposure. In the present work we investigate global pulmonary gene and miRNA expression from the same mice (Yauk et al., 2010) exposed by oral gavage for three days to BaP that exhibited no hepatic miRNA response (Yauk et al., 2010). The first goal of this work is to clarify the mechanisms of action that operate in lungs following BaP exposure via oral PD0332991 manufacturer gavage. Lung transcriptomic profiles were compared to liver profiles to identify unique pulmonary responses that may contribute to tissue-specific carcinogenicity. Second, we test the hypothesis that liver miRNAs are less sensitive to perturbations than lungs following treatment GBA3 with BaP by oral gavage. The experimental samples used in the present work were generated as part of an earlier study described in detail in Yauk et al. (2010). Hepatic mRNA and miRNA profiles were analysed in that study. However, new DNA microarrays

were run in the present study because a higher exposure dose was included here. Age matched adult male B6C3F1 mice (27–30 d, Charles Rivers Laboratories, St Constant, Quebec, Canada) were housed individually under a 12:12 h light:dark cycle with food and water available ad libitum. Mice were randomly assigned (6/group) to a control or treatment group. Mice were treated with a daily dose of BaP in corn oil with 150 or 300 mg/kg (oral gavage, 10 ml/kg) for three consecutive days. Control mice received corn oil only. Mice were anaesthetized under isofluorane and sacrificed by exsanguination at 4 h after the last treatment. Right and left lung lobes were removed and immediately snap frozen and stored at −80 °C until use. Blood serum was collected as described below. Animals have been treated humanely with due consideration to the alleviation of distress and discomfort. All animal procedures (Approval ID: 2007-005) were in accordance with the guidelines of the Canadian Council for Animal Care and approved by the Health Canada Animal Care Committee.

These observations indicated that the recombinant phospholipase-D LiRecDT1 can interact with B16-F10 membrane constituents, exhibits hydrolytic

activity toward phospholipids, and can directly metabolize phospholipids that are structurally organized on cell membranes or are extracted from B16-F10 cytoplasmic membranes to generate bioactive molecules. In spite of binding to and causing metabolism of membrane phospholipids, even under the highest purified tested phospholipase-D concentration and longest exposure time (300 μg for 72 h; a concentration sufficient to kill mice and rabbits and even cause serious problems in humans; da Silva et al., 2004; Kusma et al., 2008), the B16-F10 cells exhibited no change in viability (using Trypan ABT-263 datasheet blue

assay). Additionally, they did not suffer any type of morphological modification, such as cytoplasmic vacuolation, rounding up of cells and detaching from the substrate, cell aggregation, or cell lysis (observed through inverted microscope). These findings suggested an absence of deleterious effects of phospholipase-D on these cells as well as a lack of cellular damage, such as a breakdown of membrane integrity, under the assayed experimental conditions. Additionally, experiments using Fluo-4, which is a cell-permeant, Calcium-sensitive Selleck NVP-BKM120 fluorophore, indicated an increase in fluorescence after LiRecDT1 treatment selleck screening library (detected in two individual experimental assays: a spectrofluorimetric assay and fluorescence microscopy), demonstrating that the activity of LiRecDT1 on membrane phospholipid metabolism in B16-F10 cells could stimulate a calcium influx into the cytoplasm of the cells. This finding is in agreement with data in the literature indicating that treatment of fibroblasts with another exogenous phospholipase-D (obtained from S. chromofuscus) resulted in a cytoplasmic calcium influx ( van Dijk

et al., 1998). Moreover, the occurrence of an influx of Calcium ions inside cells following phospholipase-D treatment is supported by results showing that Calcium is required for brown spider phospholipase-D-induced hemolysis and by those of Yang et al. (2000), who reported that lysophosphatidic acid (a product generated following LiRecDT1 treatment of B16-F10 cells) induces calcium entry in human erythrocytes. Finally, the influx of ions Calcium inside cells following recombinant brown spider phospholipase-D treatment was not a consequence of leakage at the cell membrane because, as noted above, the viability of cells was unchanged, even following exposure to a high concentration of purified LiRecDT1 (as demonstrated by a Trypan blue assay detecting the breakdown of membrane integrity).

Such a high number of juveniles has never been recorded in any of the populations from other regions. Juvenile specimens were reported but never at

abundances exceeding 10% of all the individuals sampled (e.g. Ryan 1956, Rychter 1999, Roche & Torchin 2007, Fowler et al. 2013). Even though both Roche & Torchin (2007) and Fowler et al. (2013) regard juveniles as specimens with CW < 2.5 mm, their data should be taken into account, because according to López-Greco & Rodríguez (1999) and Luppi et al. (2004) acquiring maturity is a long process. Dabrafenib purchase Moreover, functional, gonadal and morphometric maturities are not always synchronised and can be reached at different stages of growth. In addition, our particular method of collection, the bottom dredge, could have contributed to the large abundance of smaller individuals as this method traps small, cryptic specimens hidden among other organisms (e.g. blue mussels or macrophytes). A high abundance of smaller individuals may indicate the reproductive success of R. harrisii in the Gulf of Gdańsk, and as a consequence, explain the demographic expansion of the target population. According to Gonçalves et al. (1995), R. harrisii larvae are produced from April to September in temperate areas. In the Gulf of Gdańsk, ovigerous females of R. harrisii were found

between June and October, just like Proteasome assay the population inhabiting Finnish coastal waters ( Fowler et al. 2013). Compared to other studies in the southern Baltic Sea (i.e.

the Dead Vistula River or the Vistula Lagoon), females in the Gulf of Gdańsk appear to produce egg masses earlier and retain them later than other populations ( Turoboyski 1973, Rychter 1999, Normant et al. 2004). While the differences may result from the application of a diversity of sampling regimes (i.e. dredging instead of traps), this extended reproductive period could be due to several environmental factors. In the Gulf of Gdańsk, R. harrisii experiences much more stable sea surface temperatures as compared to the Dead Vistula River or the Vistula Vildagliptin Lagoon, which are shallower areas that undergo rapid temperature changes ( Majewski 1972, Kondracki 2002). These fast temperature changes have been shown to impact the zooplankton communities in the Dead Vistula ( Paturej & Kruk 2011). Many crab species, including R. harrisii, exhibit sexual dimorphism with males attaining larger sizes than females – this has been observed in R. harrisii populations in the Dead Vistula River and the Odra Estuary ( Normant et al. 2004, Czerniejewski 2009). However, in the Gulf of Gdańsk population and other populations inhabiting Finland (introduced) and Louisiana (native), there were no significant size differences between the sexes ( Fowler et al. 2013). The biggest male found in the Gulf of Gdańsk was smaller than the biggest males from other populations inhabiting Polish waters ( Table 2).

There is increasing interest in adenocarcinoma of lung for various reasons. One reason is adenocarcinoma incidence is increasing (now considered to be the most predominant histologic subtype). Other reason is the potential uses of targeted therapy in cases showing EGFR mutations. Since 1980s, many studies showed EGFR over-expression in lung carcinoma particularly squamous cell carcinoma using various techniques including immunohistochemistry. However, the significance of these over-expressions as prognostic marker continued to be controversial. Clinical trials revealed variability in response to tyrosine kinase inhibitor, with higher

response seen in Japanese patients than European patients (27.5% vs. 10.4%). In USA, partial response was noticed in women, in non-smoker AZD4547 and patient with adenocarcinoma. EPZ015666 in vivo The breakthrough took place in 2004, Lynch et al. [2] reported that activating mutations of EGFR gene kinase domain resulted in responsiveness to tyrosine kinase inhibitors (TKIs) in patients with lung adenocarcinoma. Simultaneously two independent groups reported similar results [3] and [4]. Up to 20% of NSCLC shows EGFR mutation and up to 80% of these patients respond to TKIs (only 10% of EGFR mutation negative cases respond to TKIs). However, most of these patients will develop resistance to treatment within

one year [5]. Secondary resistance is either due to second EGFR mutation T790M, or MET amplification. The most frequent mutations in EGFR are exon 19 deletions and exon 21 CYTH4 point mutation: L858R (replacement of leucine at position 858 in the protein with arginine). Mutations detection start with extracting good quality DNA followed by amplifications of exon 18–21 of EGFR tyrosine kinase domain then bidirectional sequencing. The recommendation from International Association for the Study of Lung Cancer (IASLC), American Thoracic Society (ATS) and European

Respiratory Society (ERS) [6] is to test for EGFR mutation in all cases of lung adenocarcinoma, possible adenocarcinoma and NSCLC—not otherwise specified. If EGFR testing is negative, Alkfusion Test should be performed. It is optional to proceed to KRAS mutation testing (codon 12 and 13). Activating mutations in KRAS gene were shown to be of negative predictive value to TKIs. Also, KRAS mutations correlate with smoking history and poor prognosis. EGFR is a member of receptor tyrosine kinase family and a major factor in regulating cellular proliferation, invasion, metastasis, angiogenesis and inhibition of apoptosis. EGFR signals activate at least two parallel intracellular pathways [7]. One of these pathways, is the MAP kinase pathway (MAPK) that regulates G1 checkpoint in the cell cycle and control cellular proliferation [8]. Once EGFR is activated, the MAPK pathway transmits the signal to the nucleus via the active forms of RAS, RAF and MEK genes [7] and [9].

The Hospital Episodes Statistics database (HES) contains information on all admissions to an NHS hospital in England, with over 12 million new records added each year. It is managed by the NHS information center and is available for research with ethical approval. All NHS hospitals within England are required to contribute to the database. There are currently 168 acute trusts in England; however, each of these trusts can manage more than 1 hospital, and over time trusts can merge and split. Over the course of our study, Crizotinib cost approximately

150–200 providers were contributing to the database. The available data consist of a number of records for each admission, which are called episodes. Each episode represents the time period of the admission that a patient was under the clinical care of a particular consultant team during their inpatient stay. A unique patient identifier allows all records for each patient to be identified

and linked together. Each episode’s time span is defined with a start and finish date as well as being assigned an admission and discharge date for the whole period Selumetinib solubility dmso of the inpatient stay. Each episode will have up to 14 diagnoses coded using International Classification of Diseases 10th revision (ICD-10); and up to 12 procedures coded using the United Kingdom Tabular List of the Classification of Surgical Operations and Procedures (OPCS) (version OPCS4). This database has been linked to the Office of National Statistics (ONS) death register since 1998. All admissions older than 15 years Methocarbamol (chosen to be consistent with the lower age limit of previous British Society of Gastroenterology (BSG) audits of mortality in gastrointestinal hemorrhage8 and 9), which had an ICD-10 code for upper gastrointestinal hemorrhage, with a date of hemorrhage between January 1, 1999, and December

31, 2007, were extracted. Data were available for 2008 to allow complete follow-up of mortality for admissions occurring in December 2007. Upper gastrointestinal hemorrhage was defined as an ICD-10 code that specifically implied either variceal gastrointestinal hemorrhage: esophageal varices with hemorrhage (I85.0) or nonvariceal hemorrhage: Mallory–Weiss syndrome (K22.6), esophageal hemorrhage (K22.8) acute, or chronic gastric ulcer with hemorrhage including perforation with hemorrhage (K25.0, K25.2, K25.4, K25.6), acute or chronic duodenal ulcer with hemorrhage including perforation with hemorrhage (K26.0, K26.2, K26.4, K26.6), acute or chronic peptic ulcer with hemorrhage including perforation with hemorrhage (K27.0, K27.2, K27.4, K27.6), acute or chronic gastrojejunal ulcer with hemorrhage including perforation with hemorrhage (K28.0, K28.2, K28.4, K28.6), hematemesis (K92.0), melena (K92.1), or unspecified gastrointestinal hemorrhage (K92.2). This ICD-10 code list has previously been used in hospital data.

Kukliński, P. Bałazy and the officers and crew of the r/v ‘Oceania’ for their assistance at sea. We thank especially Prof. Stanisław Massel, who provided numerical simulations, and Dr K.W. Opaliński helped a lot in the final shaping of the

discussion and the present version of the manuscript. “
“The Editor would like to thank every reviewer who cooperated by evaluating the papers submitted to Oceanologia in 2011. We have received kind permission to print the following reviewers’ names: ■ Dr David G. Adams (University of Leeds, United Kingdom) “
“The underwater light field is a major factor affecting the composition and quantitative characteristics of phytoplankton pigments in the environment. Changes in light intensity and its spectral distribution in the water body govern the physiological acclimation of phytoplankton cells (Harrison and Platt, 1986 and Falkowski and selleck compound LaRoche, 1991). These adjustments lead to morphological changes in algae cells, i.e. a change in volume and the number of thylakoid membranes – by up to 50% (van Leeuwe & Stefels 1998), and a resizing of the different cellular structures (Sukenik et al. 1987). As a result, the contents of pigments and lipids

and their composition in the cells of algae and cyanobacteria change (Berner et al., 1989 and Falkowski and LaRoche, 1991), which implies that the absorption characteristics of marine algae (Bricaud et al., 1983, Sathyendranath et al., 1987 and Stramski et al., 2002), and by extension the quantum yield of photosynthesis (Morel et al. 1987) must have changed, too. The nature of the underwater light field affects the intercellular content of the photosynthetic (PSP) and photoprotective (PPP) pigments by Crizotinib various types of photoadaptation, which enables organisms to achieve the most efficient absorption of light quanta for use in photosynthesis (Babin et al., 1996, Woźniak et al., 2003, Woźniak and Dera, 2007 and Dera and Woźniak, 2010). These processes may occur as a result of the high intensity of http://www.selleck.co.jp/products/Verteporfin(Visudyne).html blue light in the surface water layer, which would cause photooxidation

of chlorophyll a, or of the presence of a narrow spectral irradiance at different depths, which prevents the chlorophyll a molecule from directly absorbing light quanta. In the first case, the cells produce larger amounts of protective pigments (intensity adaptation, also called photoadaptation), while in the second case, they support the production of additional pigments (antenna pigments), which permit the more efficient utilization of solar energy through photosynthesis (chromatic acclimation). In both cases the modifications affect not only the concentration of pigments in the cells, but also their relative content (i.e. the ratio Ci/Cchl a, where i denotes the relevant pigment), determining the vertical distributions of the relative content of PSP and PPP in the water body ( Schlüter et al., 2000, Henriksen et al., 2002 and Staehr et al., 2002). Photoacclimation is a highly dynamic process.

Following from the issues raised by direct contact between EC and fibroblasts, barrier effects of filters and gel contraction, we developed a ‘double gel’ model. This provided a contiguous system of cells and tissue-like matrix that might be more physiologically

relevant than our alternative models. Under these conditions, fibroblasts enhanced the numbers of lymphocytes migrating through the EC, but had no effect on their subsequent migration potential through the gel. Thus, the results supported the conclusion that fibroblasts promoted transendothelial migration of PBL through remote effects of soluble mediators but influenced penetration of tissue mainly by modifying matrix structure. Few PBL reached the fibroblast zone after 24 h in this construct, learn more and it would be necessary to either reduce the thickness of the upper gel layer or extend the duration of the assay, to test whether fibroblasts could influence motility of lymphocytes by direct contact. In all of the models, ability to retrieve Forskolin mouse cells that have migrated into the different regions allowed us to study differential responses of lymphocyte subsets without costly and potentially property-changing pre-isolation procedures. Using immuno-labelling and flow cytometry, we were able to show that T-cells (CD4 and CD8) and B-cells

migrated across endothelial mono and co-cultures with equal ability in the two models examined (multi-filter and filter-gel). Moreover, effector memory T-cells showed an enhanced migratory capacity, preferentially migrating through EC. Thus the process of transendothelial Thiamet G migration does not appear to be selective at the level of T- and B-cells, but could potentially select for discrete subpopulations such as effector memory. Interestingly, migration of T-cells, but not B-cells, into matrix or through the stromal-filter layer was adversely affected

by the presence of fibroblasts. In light of the above, these findings suggest that it is the migration potential of T-cells that is sensitive to modifications in the matrix structure. It is possible that B-cells may be better able to remodel the matrix to create pathways for their entry making them less sensitive to structural changes within the matrix. An alternative explanation is that fibroblast-derived mediators are more attractive to B-cells than T-cells. For example, it has been reported that B-cells adhere more efficiently to human dermal fibroblasts than T-cells (Couture et al., 2009). Moreover, B-cells, but not T-cells, were able to migrate through a fibroblast barrier (monolayer) (Couture et al., 2009). In fact in that study the fibroblasts appeared to selectively promote B-cell migration. Our understanding of comparative lymphocyte (T-cell vs. B-cell) migration through tissue matrix during inflammation is limited and requires further investigation.

A smaller study (N = 39) by the same group reported no differences in patient survival, graft survival, or BPAR incidence between patients receiving SRL/standard TAC and those receiving SRL/reduced TAC (Table 1) [49]. However, 38% and 6% of patients on standard TAC were discontinued due to TAC nephrotoxicity and thrombotic microangiopathy, respectively. Several factors may have contributed to the apparent increased nephrotoxicity, including the study population (79% black), use of kidneys from deceased

donors, and high incidence of delayed graft function (59%). Two-year data compared similar regimens in 132 live donor renal allotransplant patients [50]. The efficacy outcomes were patient survival and graft

survival, BPAR incidence, and graft function. At 2 years, renal function MK-1775 nmr was significantly improved with the TAC-free regimen (SRL/MMF), compared with see more the SRL/TAC-sparing regimen, as measured by serum creatinine level and calculated GFR (both p < 0.05; Table 1). In addition, the rate of acute rejection was numerically lower in the TAC-free group (13.5% vs 18.5%; p = ns). Three-year results from a long-term study (N = 150) comparing SRL/TAC, MMF/TAC, and SRL/CsA are also available [51]. At 3 years, patient survival, graft survival, and BPAR incidence did not differ significantly among the 3 groups (Table 1), although the latter showed a trend in favor of MMF/TAC (p = 0.07). Although renal function (as measured by creatinine) was acceptable in each of the 3 groups, the MMF/TAC group was statistically more favorable when compared with SRL/CsA at 12, 24, and 36 months

(p = 0.02, p = 0.05, ROS1 and p = 0.04, respectively) and SRL/TAC at 24 months (p = 0.05). Rates of NODM by year 3 were lowest with MMF/TAC (11% vs 27–31% in other groups). Longer-term follow-up of the same study (median of 8 years) showed significant differences or trends with respect to the above endpoints that consistently favored MMF/TAC over the other regimens [52]. Viral infections and need for antilipid therapy were significantly lower with MMF/TAC versus the other regimens combined (p < 0.05), and the incidence of NODM was numerically lower with MMF/TAC (Table 1). Similar long-term findings were reported by Chhabra and colleagues [53]. In their study, 82 renal transplant recipients were followed for up to a mean of 8.5 years. MMF/TAC provided better efficacy and safety than SRL/TAC, with significant differences seen for graft survival and GFR (Table 1). In summary, results to date are derived mainly from single-center studies, and thus more robust data are needed to confirm the preliminary findings. Two small-scale studies compared reduced-dose TAC versus standard-dose TAC, when used in combination with SRL [47] and [49].

Using a repeated measures design, the rats (n = 6) received water, DON (2.0 mg/kg b.w.) and the equimolar amount (6.8 μmol/kg b.w.) of D3G (3.1 mg/kg b.w.) by gavage on days 1, 8 and 15 of the experiment, respectively. Stock solutions of 400 μg/mL DON and 619 μg/mL D3G were prepared by dissolving the solid standards in water. Thereof, volumes of 1.4–1.8 mL were administered to the rats according to

their weight. Feed was withdrawn 12 h before the treatment. After administration, the animals were housed individually in polycarbonate metabolic cages (Tecniplast, Hohenpeißenberg, Germany) for 48 h. Urine and feces were collected for the periods 0–24 h and 24–48 h after dosing and volumetrically measured or weighted, respectively. The samples were frozen at −20 °C at the check details end of the 48 h period. The study design was approved by both, the Ethics Committee of the Medical University of Vienna and the Austrian Ministry for Science and Research. Urine samples were centrifuged (10 min, 14,000 × g), acidified with 1% of acetic acid and cleaned up by solid phase extraction (SPE) on Strata C18-T cartridges (200 mg, Phenomenex, Aschaffenburg, Germany). After conditioning of the

cartridges with 5 mL of MeOH and 5 mL of MeOH/water/acetic acid (5/94/1, v/v/v), 500 μL of urine samples containing 1% of acetic acid were applied. Subsequently, the cartridges were washed with 1 mL of MeOH/water/acetic acid (5/94/1, v/v/v). The analytes were eluted with 2 mL of MeOH/water/acetic acid (70/29/1, v/v/v) selleck screening library and the eluates were evaporated to dryness under compressed air. The residues were reconstituted in 5 mL of ACN/water (20/80, v/v) for LC–MS/MS analysis. Feces samples were freeze-dried,

homogenized and 250 mg aliquots were extracted three times (40/40/20 min) with MeOH/water (50/50, Coproporphyrinogen III oxidase v/v, 3/2/2 mL) on a GFL rotary shaker (Burgwedel, Germany). 500 μL aliquots of the pooled raw extracts were combined with 500 μL cold MeOH. Subsequently, the solutions were vortexed for 15 s and centrifuged at 9000 × g for 10 min. Finally, 300 μL of the supernatants was evaporated to dryness under compressed air and re-dissolved in 300 μL of MeOH/water (20/80, v/v). The samples were vortexed for 30 s and clarified by centrifugation (10 min, 14,000 × g) for LC–MS/MS analysis. Clean-up procedures for feces and urine as described above resulted in sample dilutions by a factor of 56 and 10, respectively. Analysis was performed on an 1100 series high performance liquid chromatography (HPLC) system (Agilent Technologies, Waldbronn, Germany) coupled to a QTrap 4000 LC–MS/MS System (AB Sciex, Foster City, CA) equipped with a Turbo V electrospray ionization (ESI) source. Chromatographic separation was achieved on an Atlantis® T3 column (3.0 mm × 150 mm, 3 μm, Waters, Vienna, Austria) equipped with a 4 mm × 3 mm C18 security guard cartridge (Phenomenex, Torrance, CA, USA). Eluent A was composed of water/acetic acid (99.9/0.

In addition, there are some gaps in the data for technical reasons: from 16 August 1989 to 7 November 1991, from 15 December 1992 to 14 September 1994, and from 10 November 1994 to 4 October 1995. The shore at CRS Lubiatowo has a gently sloping beach from several to tens of metres wide. The dune toe lies from 1 to 2 m above the mean water level, whereas all points of the dune crest are at least 2 m higher than the dune toe

(adjacent to the landward edge of the beach). Locally, there is a small beach berm near the shoreline. Both the beach and dunes consist of fine quartz sand with a median grain diameter of around d50 ≈ 0.22 mm. Since there are practically no tides (a maximum of 6 cm), swell and wind waves are the only drivers of water motion in the nearshore Ibrutinib zone. The complex shape of the sea bed (see the example of a multi-bar cross-shore transect in Figure 2) causes multiple wave breaking and

the Trametinib cell line dissipation of much wave energy over the bars. According to investigations by Pruszak et al. (2008), only about 40% of the wave energy actually reaches the immediate proximity of the shoreline. The sea bed on the shore section of interest is characterized by bars, of which there may be from 3 to 5. The first stable bar is located at about 100–120 m, the second bar about 250 m and the third one 400–450 m from the shoreline; the fourth and fifth bars occur (sometimes as a single morphological entity) at a distance of 650–850 m offshore. In addition, there is often one more irregular sea bed form very close to the shoreline – a flat shoal that migrates in

various directions and disappears periodically. The shoreface has a mean slope of tan β = 0.015 (locally, at the shoreline, with a maximum of 0.04). The complicated nature of this coastal area, implying complex hydrodynamic and lithodynamic processes, is illustrated in Figure 3. Since 1983, geodesic surveys of the dunes and beach have been carried out every month along the 2.6 km section of shore. The tachymetry comprises cross-shore profiles every 100 m along the shore. This gives 27 measured transects. The results of the field investigations described above are plotted in Figure 4. The data comprising, by way of example, a short-term annual period from for September 2006 to September 2007 are shown in Figure 4a, whereas the data collected during the entire 25 year time span (1983–2007) are shown in Figure 4b. The shoreline position, interpreted as the distance of the shoreline point from a certain geodesic baseline, is denoted by ys, while the dune toe position, interpreted as the distance of the dune toe point from the geodesic baseline, is denoted by yd. Figure 4 shows that the range of shoreline migration ys is much larger than the range of changes of dune toe position.