An 1100 Series HPLC System (Agilent, Waldbronn, Germany) in conjunction with a QTrap-LC–MS/MS System (Applied Biosystems, Foster City, USA) equipped with a Turbo Ion Spray source were used for analysis. Isocratic separation of the compounds was achieved using methanol/water (25/75, v/v) containing 5 mM ammonium acetate, at 22 °C in a 100 mm × 4.6 mm, 3 μm, RP-18 Aquasil column (Thermo, Bellefonte, PA, USA). 10 μL sample volume was injected into a flow of 0.5 mL/min. The negative ion mode was selected for analyte ionization. ESI parameters were as follows: source temperature 400 °C, curtain gas 20 psi (138 kPa), nebulizer gas 30 psi (207 kPa), auxiliary gas 75 psi (517 kPa),

ion spray voltage Histone Methyltransferase inhibitor −4200 V, CAD gas 6 (arbitrary units), MRM dwell time 50 ms, pause between mass ranges 5 ms. The MRM transition of m/z 517.1 to m/z 59.1 (DP −32 V, CE −81 eV) was chosen for D3G, while m/z 355.1 to m/z 59.1 (DP −16 V, CE −30 eV) was chosen for DON. Qualifier transitions were taken from the original LC–MS/MS method ( Berthiller et al., 2005). In order to determine the fate of D3G upon ingestion by mammals, in vitro experiments mimicking the digestion conditions IPI-145 cost in the gastrointestinal tract were performed. Control experiments proved the stability of the precursor mycotoxin, DON, at all investigated

conditions. Furthermore, the sum of the molar amount of DON and D3G remained roughly constant (within 10%) in all experiments, indicating no losses of toxins during the experiments. Acidic solutions were used to assess the impact of the conditions found in the stomach of mammals on D3G stability. D3G proved to be completely stable towards acid hydrolysis with 0.02 M HCl, at a pH-value of about 1.7, which is at the lower end of the stomach pH range in humans. Even at a 10 times higher concentration of HCl, at a pH-value of about 0.7, no DON could be detected after incubation of D3G at 37 °C for 3 h or 18 h. Artificial stomach juice, containing pepsin at pH 1.7, also had no effect on D3G. The results of the hydrolysis studies under acidic and enzymatic conditions

(see below) are summarized in Table 1. In all acid-treated samples 100 ± 2% of D3G were recovered. A variety of glycosylhydrolases was used to test the enzymatic stability of D3G. Artificial (non-microbial) gut juice, containing amylase, showed no activity selleck screening library at all towards the β-glucoside D3G. Similarly, while testing 1 U/mL of almond β-glucosidase, no activity (<0.01 mg DON/L) was noticed towards D3G. This is in agreement with results obtained previously for D3G (Sewald et al., 1992) while Z-14-G was completely converted to ZEN (although at higher enzyme concentrations) by this enzyme (Gareis et al., 1990). More importantly, also human cytosolic β-glucosidase (hCBG, expressed in Pichia pastoris) did not show any activity for D3G. β-Glucuronidase, commercially purified from snail gut, can cleave β-glucuronides, but also possesses high β-glucosidase and arylsulfatase side activities.

, 1992), and protistan grazing (Hartke et al., 2002). What is often absent from efforts to understand nearshore FIB persistence, however, are syntheses of physical and biological dynamics. Only a handful of studies have attempted to quantify the importance of different physical or biological processes in controlling the extent and intensity of FIB pollution in the surfzone (Boehm et al., 2005, Boehm et al., 2009 and Grant et al., 2001). Even fewer use models as vehicles to test hypotheses concerning the accuracy with which different combinations of mechanisms can reproduce actual FIB data (Boehm, 2003, Boehm et al., 2005 and Sanders et al., 2005). Here, we present a study designed

specifically for this purpose. Data were acquired during a 5-h field program at Huntington Beach, CA, on October 16th, 2006, that monitored nearshore FIB concentrations, AZD6244 cost waves,

and currents. In this manuscript we explore the role of biological dynamics (in this case mortality) in controlling the spatial and temporal variability of FIB at Huntington Beach. Six different mortality functions representing different FIB mortality mechanisms are added to an individual based model of FIB that contains alongshore advection and cross-shore variable horizontal diffusion (the AD model). These new mortality models, together with additional data CHIR-99021 manufacturer (Enterococcus species distribution and time dependent solar insolation dose observations), are used to evaluate hypotheses regarding FIB mortality mechanisms in the nearshore. The mortality mechanisms explored in this paper are: spatially and temporally constant mortality

(null hypothesis), spatially constant solar-induced mortality, stationary cross-shore mortality gradients, FIB source-dependent mortality, and two combinations of the above. Solar-induced mortality was explored because insolation is often posited as a dominant source of mortality for nearshore FIB, and has been suggested to affect FIB at Huntington Beach (Boehm et al., 2002 and Sinton et al., 2002). Cross-shore mortality gradients were examined because surfzone and offshore waters often have different dynamics, which can result in cross-shore gradients of properties affecting FIB mortality, like temperature, grazers and turbidity (Omand et al., 2011, Reniers et al., 2009 and Smith and Largier, 1995). Turbidity gradients, in particular, can affect Anacetrapib the penetration of solar insolation, which, if FIB are solar sensitive, may result in cross-shore variable FIB mortality gradients that the organisms move through as they are advected and diffused across shore (Alkan et al., 1995 and Whitman et al., 2004). One of our two combination mortality functions includes both cross-shore mortality gradients and solar sensitivity to depict this particular mortality mechanism. Lastly, source-specific FIB mortality was examined because FIB from different sources can have different mortality rates (Sinton et al.

Any laboratory can then compare their own genotypes to the baseline R428 to assist in assigning individuals to population. Given the number of SNP markers found in eukaryotic genomes, the potential to develop targeted SNP assays for specific traceability issues is good. This is particularly the case in many commercially

exploited marine species where population sizes are large meaning selection is relatively powerful in comparison to genetic drift. The FishPoptrace project has developed and tested a range of traceability tools for assigning fish and fish products back to population of origin (SNPs, otolith shape and microchemistry, gene expression, proteomics). SNPs were identified as the only tool that could be used at every stage of the food chain, from freshly caught fish though to processed fish products such as canned or other processed products. SNPs were developed and tested in three species (herring, sole, and hake) and existing SNP markers were tested in cod. SNPs allowed high levels of assignment to population of origin – with a small subset of SNP learn more markers providing ‘maximum power for minimum cost’ (Nielsen et al., 2012).

Moreover, all protocols were forensically validated. In this study, SNPs for herring, sole and hake were identified through 454 sequencing (Roche 454 GS FLX sequencer) of the transcriptome. By using gene-associated single nucleotide polymorphisms, it was shown that individual marine fish can be assigned back to population of origin with unprecedented high levels of precision. By applying high differentiation single nucleotide polymorphism assays, in four commercial marine fish, on a pan-European scale, 93–100% of individuals could be correctly assigned to origin in policy-driven case studies. The authors

show how case-targeted single nucleotide polymorphism assays can be created and forensically validated, using a centrally maintained and publicly available database. The results demonstrate how application of gene-associated markers will likely revolutionize origin assignment and become highly valuable tools for fighting illegal fishing and mislabelling worldwide Interleukin-3 receptor (Nielsen et al., 2012). Transcriptomics comprises, amongst other methods, the analysis of gene expression changes (as measured by the amount of RNA from a particular gene) of either an entire organism or part of it (e.g. cells, tissues) under different conditions (e.g. at different developmental stages or upon exposure to chemicals or stressors). The most common technologies used to investigate gene expression changes are DNA microarrays, quantitative real time PCR (qRT-PCR) (Lettieri, 2006) and RNAseq (Montgomery, 2010). A DNA microarray is a glass or a nylon membrane on which parts of gene sequences (oligonucleotide probes) are spotted. The fluorescently labelled RNA extracted from organisms, organs (e.g. liver) or cells exposed to a pollutant/stressor is hybridized against the array.

Despite many controversies, several studies have shown that there is a relationship between obesity and the increase in bone mass.8 and 9 Bone tissue is highly dynamic and is in a constant state of change, basically due to three processes: bone growth, modelling and remodelling. The latter is a continuous physiological process that allows the maintenance of bone strength and it is Sorafenib regulated by the interaction amongst bone cells and a variety of systemic hormones, cytokines, growth factors and inflammatory mediators. Obese individuals have higher bone mineral density (BMD) than non-obese individuals, and this may be a protective factor

against osteoporosis and fractures.10 Obesity may inhibit hepatic synthesis of the insulin-like growth factor binding proteins (IGFBP-3). IGFBP-3 is normally

associated with hyperinsulinemia and promotes greater activity of the insulin-like growth factor (IGF-I), which together with the direct activation of IGF-I receptors by insulin stimulate the proliferation of osteoblasts.11 and 12 Several studies have shown that leptin, a hormone secreted mainly by the adipose tissue, may have an important osteogenic effect on pubertal development and skeletal maturation.9 Other studies have indicated that if this hormone is administered directly on the cerebral ventricles of leptin-deficient mice, it may cause bone loss.8 Vorinostat chemical structure However, other authors concluded that leptin is a physiological anti-resorptive factor and it plays a role in the protective effects on bone mass.13 To study the origins of obesity and its pathological consequences, different experimental models of obese animals have been used, and amongst them, the one induced by monosodium glutamate (MSG) treatment. The administration of MSG in rats and mice during the first days after birth causes lesions in the arcuate nucleus and median eminence of the hypothalamus,14 and 15 altering the normal functioning of the hypothalamus–hypophysis axis. These animals are characterised by presenting deficiency

in the Farnesyltransferase release of the growth hormone16, 17 and 18; reduced basal metabolic rate, with increase in lipogenesis and diminished lipolysis19; hypo- or normophagia; obesity; hyperinsulinemia20 and 21; insulin resistance20 and increase in corticosterone and leptin concentrations.22 Several studies have been conducted to investigate the relationship between obesity and several chronic-degenerative diseases that accompany this epidemic. Nevertheless, despite evidence showing the interrelationships amongst obesity, bone remodelling and periodontal disease, the literature is very restricted, requiring much research in this scientific field. The aim of this study was to evaluate the relationship between the model of obesity induced by neonatal MSG treatment and induced periodontal disease.

The authors assumed that rmax=2 M [61], where M (the natural mortality rate) is estimated from Hoenig’s [62] empirical equation based on observed maximum age. If no maximum age was known, the authors used the von Bertalanffy growth parameter

K and followed Jensen’s MK-2206 ic50 [63] suggested approximation with M=3/2K. Table 1 generally suggests that very low resilience/productivity (i.e. high vulnerability) is typical of deep-sea fishes, including species that are commonly exploited by deep-sea fisheries. The estimated rmax of the deep-sea species the authors studied has a mean value of less than 0.37 year−1, with high intrinsic vulnerability (i.e., index>60). Similarly, species commonly exploited by deep-sea fisheries have low average rmax of 0.314 year−1. Further, these have markedly lower rmax and higher intrinsic vulnerability index than non-deep-sea fishes (i.e., species generally found shallower than 200 m) of similar length ( Fig. 2). This agrees with results from previous assessments that deep-sea demersal fishes, particularly those that aggregate around seamounts, are more vulnerable than other fishes [24] and [28]. Maximum body size alone may not be a good indicator of resilience or vulnerability to fishing because some of the highly vulnerable species are not large. These metrics of resilience and intrinsic vulnerability, specifically

rmax, can be compared to economic metrics to evaluate Apoptosis inhibitor the sustainability of deep-sea fishing. In species where recruitment is more or less stable at population sizes above 50% of unexploited size, a reasonable assumption for many low-productivity species, the maximum intrinsic growth rate rmax=2M, where M is the natural mortality rate. This

leads to a target fishing mortality rate for maximum sustainable yield (MSY) of Fmsy=M. For species that have maximum ages of 30 years or greater, M is however expected to be<0.1; thus, maximum fishing mortality rates under standard management models must also be <0.1, a difficult target to meet in open-access fisheries. If a local stock or population is depleted (F⪢Fmsy) and does not receive significant recruitment from unexploited sources, the chances of local extinction are extremely high. Species with restricted geographic range and aggregation behavior are particularly vulnerable to overfishing [46], [55] and [64]. Many deep-sea fishes that inhabit seamounts naturally aggregate for feeding and spawning. These species include orange roughy, splendid alfonsino (Beryx splendens), alfonsino (Beryx decadactylus, Berycidae), blue ling (Molva dypterigia, Lotidae) and slender armourhead (Pseudopentaceros wheeleri, Pentacerotidae). The level of population connectivity among seamounts is unknown for most species but recolonization rates may be very low or episodic [43]. This further reduces their resilience to fishing [24]. With a million dollars capital (=principal) in the bank, one can withdraw $30,000 per year in perpetuity at a guaranteed 3% annual interest rate.

5% FCS) on 24-well collagen-coated culture plates. Effectene Transfection Reagents were prepared in glia culture medium (without antibiotics/antimycotics) and added drop-wise to the cells. The transfection method was optimized by testing the effects of: the number of cells added, prolonged incubation time, and removal of complexes after 16 h (data not shown). Cells were incubated with transfection complexes

for 24 h. After incubation, cell supernatants and extracts were collected for further use. Primary astrocytes were isolated as previously done (Wiesenhofer and CDK inhibitor Humpel, 2000 and Zassler et al., 2005a) and used as a positive control. Primary cultures of freshly isolated rat monocytes were transiently transfected with pEF-NGF plasmid using FuGene HD Transfection Reagent (Promega) according to manufacturer’s instructions.

Briefly, cells were seeded 1 × 105 cells per well in medium (without antibiotic/antimycotics). Cells were incubated at 37 °C until reaching 80% confluency on the day of transfection. On the day of transfection, the DNA-FuGENE mix was prepared in Optimem (Gibco) and added drop-wise to the cells. Different concentrations of DNA, amount of FuGENE EX 527 solubility dmso HD reagent, incubation times with transfection mix, ‘boosting’ with transfection mix, and recovery times were also evaluated (data not shown). Cells were incubated with transfection complexes for 24, 48, or 72 h in Amaxa culture medium (10% FCS, 2 mM glutamine, 1 ng/ml M-CSF, 1 ng/ml GM-CSF). After incubation, cell supernatants were collected for further use. Primary cultures of freshly isolated rat monocytes were nucleofected with pEF-(−), pmaxGFP, or pEF-NGF using the Human Monocyte Nucleofection kit (Amaxa) according to the manufacturer’s instructions. Monocytes were pelleted directly following isolation at 250 ×g for 5 min. Cell pellets

were resuspended in 110 μl of Nucleofector solution (Amaxa), mixed with plasmid DNA, and transferred to an Amaxa cuvette. Nucleofection was performed using the Amaxa program Y-001. Control samples were nucleofected using Adenosine the empty vector (pEF-(−)). Immediately following nucleofection, 500 μl of pre-warmed glia culture medium (Optimem I, 5% horse serum, 0.5% FCS) (without antibiotics/antimycotics) or Amaxa culture medium (10% FCS, 2 mM glutamine, 1 ng/ml M-CSF, 1 ng/ml GM-CSF) was added to the cuvette and subsequently transferred to a collagen-coated 24-well culture plate. Nucleofected cells were incubated for 1–2 days at 37 °C 5% CO2. After incubation, cell supernatants and extracts were collected for NGF ELISA or cells were stained for further microscopic analysis. Primary astrocytes were isolated as previously done ( Wiesenhofer and Humpel, 2000 and Zassler et al., 2005a) and used as a positive control.

The paucity of collagenesis and microangiogenesis in nonpolypoid adenomas suggest that these 2 molecular signals are either inadequately or not elaborated, elaborated but not released, or locally abrogated.18 Intraepithelial lymphocytes (IELs) are often seen in polypoid and nonpolypoid adenomas. Nonpolypoid adenomas with HGD contain more IELs than those with LGD, implying that the degree of IEL infiltration increases with increasing degree of dysplastic severity and/or with the increasing biologic age of the adenoma. Notably, 38% of the nonpolypoid adenomas exhibited a subjacent lymphoid aggregate.19

It is not inconceivable that lymphoid aggregates might evolve as an immunologic mucosal response, as do occur in newly formed lymphoid aggregates in CC.20 Intraepithelial granules see more (Leuchtenberger bodies) are often found in polypoid and nonpolypoid adenomas. In a survey, 84% of the nonpolypoid (flat) adenomas exhibited apoptotic granules. The overwhelming majority of the apoptotic granules

were seen in the subnuclear basal aspect of the dysplastic cells facing the basement membrane, denoting that the cells responsible for the apoptotic granules were to be found in the vicinity of the lamina propria normally infiltrated by lymphocytes.21 Direct immunoperoxidase detection of nuclear DNA fragmentation and transmission electron microscopy comfirmed that these DNA-containing bodies were apoptotic (nuclear) Cabozantinib solubility dmso fragments from disintegrated lymphocytes, and not nuclear remnants from dead dysplastic cells.22 In fact, dysplastic cells remained undamaged (as deduced from transmission electronmicroscopy and nuclear DNA proliferation markers). Semiquantitative Erastin nmr assessments of apoptotic granules showed that the number of flat adenomas with excessive granular density was highest amongst those with HGD. Hence, apoptosis in nonpolypoid adenomas might express a mechanism of cell defense, whereby neoplastic cells inflict

apoptosis on IEL in advanced nonpolypoid adenomas, through the Fas-FasL pathway.23 Importantly, the frequency of apoptotic granules in flat adenomas is similar in Japan and Sweden, implying that apoptosis in those lesions neither is influenced by race nor by the environment. The authors demonstrated a low K-ras mutation rate in flat adenomas. Cancers arising de novo were significantly associated with loss of heterozygosity at chromosome 3p. 24 The chronologic appearance of flat adenomas was traced in a cohort of rats injected with dimethylhydrazine (DMH). Flat adenomas developed earlier (week 13) than polypoid adenomas (week 15). Flat adenomas were more numerous on week 19, whereas polypoid adenomas were more numerous on week 22.

In the region of the nucleus that faces the centrioles a depression is formed, the nuclear fossa, which totally or partially houses the centrioles. In Type III spermiogenesis (Quagio-Grassiotto et al., 2005 and Quagio-Grassiotto and Oliveira, 2008), at the beginning of the differentiation process, the centrioles are anchored at the plasma membrane in a position medial to the nucleus. The centriolar migration does not occur and neither does the nuclear rotation. The cytoplasmic canal may or may

not be formed. When it does occur, the formation of the cytoplasmic canal is due to the movement of the midpiece cytoplasm in the direction of the initial segment of the flagellum. Alternatively, it may be due to the formation of vesicles at the midpiece terminal end that project http://www.selleckchem.com/screening/selective-library.html in the direction of the initial segment of the flagellum. Variations in Type III spermiogenesis are found in Callichthyidae, subfamily Corydoradinae (Spadella et al., 2007). Here the centriolar complex is strongly eccentric PR-171 in vivo in relation to the nucleus. Consequently flagellum development also occurs in an eccentric position. The centrioles do not migrate and the nuclear rotation does not occur. A

shallow nuclear fossa is formed, but the centrioles stay outside. T. paraguayensis has a classical spermiogenesis of Type III in which the nuclear fossa is never formed and the cytoplasmic canal results from the projection of the midpiece vesicles in the direction of the initial segment of the flagellum. Spermiogenesis has peculiar characteristics in the two other doradids examined herein. Spermiogenesis in A. weddellii is a variation of Type III (i.e., Type III modified). The initial position of the centrioles is medial to the nucleus, and the absence of nuclear rotation characterizes spermiogenesis as Type III. The formation of the nuclear fossa and the cytoplasmic canal are due to the simultaneous projection

of the nucleus and cytoplasm toward the initial segments of the flagella and to the migration of the centrioles forward towards the tip ever of the nucleus. P. granulosus and R. dorbignyi have a classical spermiogenesis of Type I in which nuclear rotation is complete and centriolar migration occurs. Spermiogenesis in O. kneri is a variation of Type I, in which the nuclear rotation is complete; however, the centrioles do not migrate. In O. kneri the nuclear fossa is formed by the projection of the nucleus toward the centrioles, whereas the cytoplasmic canal results from the projection of the cytoplasm toward the initial segment of the flagellum. The different types of spermiogenesis, Types I and II (Mattei, 1970) and Type III (Quagio-Grassiotto et al., 2005 and Quagio-Grassiotto and Oliveira, 2008) characterize the extremes. As previously noted by Mattei (1970), variations in these processes are conducive to the formation of intermediate types of sperm, mainly considering the orientation of the flagellum in relation to the nucleus.

Na przegrodę serca, poza przegrodą międzyprzedsionkową, składają się przegroda przedsionkowokomorowa i przegroda międzykomorowa. Tworzenie tej drugiej jest ściśle związane z

rozwojem zastawek przedsionkowo-komorowych i pozostałych części przegrody serca. Kanał przedsionkowo-komorowy, który stanowi połączenie między wspólnym przedsionkiem a komorami serca, ulega zamknięciu za sprawą uwypukleń w dolnej i górnej części, zwanych poduszeczkami PFI-2 mw wsierdziowymi (Ryc. 4). Ich wzrastanie doprowadza ponadto do zamknięcia otworu pierwszego, częściowo pierwotnego otworu międzykomorowego oraz wytworzenia oddzielnych pierścieni zastawek przedsionkowo-komorowych – trójdzielnej

i dwudzielnej (mitralnej) [19, 20]. Rozwój tych ostatnich zależy jednak również od poduszeczek wsierdziowych bocznych, które je „uzupełniają”. Na drodze DZNeP in vivo powyższego procesu tworzy się również część błoniasta przegrody serca, składająca się z dwóch części – przegrody przedsionkowo-komorowej i części błoniastej przegrody międzykomorowej [11, 19]. W tym miejscu należy zaznaczyć, że przez wiele lat uważano, iż przegroda przedsionkowo-komorowa jest strukturą zbudowaną z dwóch części – mięśniowej i błoniastej. Najnowsze doniesienia i doświadczenia autorów artykułu potwierdzają jednak, że właściwą przegrodą jest jedynie część błoniasta 24., 25. and 26.. Dawniej używane określenie części mięśniowej odnosi się wyłącznie do miejsca,

w którym ściana prawego przedsionka położona jest na ścianie lewej komory, a pomiędzy nimi znajdują się naczynia (m. in. tętnica węzła przedsionkowo-komorowego) otoczone tkanką łączną [24]. Wytworzenie oddzielnych pierścieni zastawek przedsionkowo-komorowych nie jest jednoznaczne z rozwojem aparatu zastawkowego – ich płatków, strun ścięgnistych i mięśni brodawkowatych. Te powstają na drodze odsznurowania się od wewnętrznych ścian before komór na drodze apoptozy, co oznacza, że pod względem embriologii i morfologii należą właśnie do komór 27., 28. and 29.. Sprawia to, iż niezależnie od położenia komór i morfologii łączących się z nimi przedsionków, zastawka trójdzielna będzie obserwowana w obrębie komory morfologicznie prawej, a dwudzielna w komorze morfologicznie lewej. Niecałkowite odsznurowanie się płatków zastawek przedsionkowo-komorowych prowadzi do rozwoju zespołu Ebsteina, kiedy to dochodzi do dokoniuszkowego przemieszczenia płatków zastawki trójdzielnej (Ryc. 5). Mięsień komór ulega w trakcie rozwoju licznym przekształceniom. Stopniowe uwypuklanie komór doprowadza do poszerzenia ich światła oraz wytworzenia dolnej części przegrody międzykomorowej. Jeszcze w 7.

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 PF-06463922 in vitro 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 CTLA-4 antibody 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 aminophylline 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.