The strategy of this study is to perform a large-scale analysis of gene expression in order to highlight possible regulation pathways differentiated by traumatic occlusion in early phase. The experiment was conducted with male SD rats (250 ± 10 g) from Laboratory Animal Centre of Shandong University (Jinan, China). The animals were housed under conditions of controlled temperature (23 ± 2 °C) and humidity (60%) with natural light. The experimental protocol was developed according to the see more institution’s guideline for the care and use of laboratory animals. Anaesthesia was accomplished using chloral hydrate 40 ml/kg (Qilu

Hospital in Shandong University, Jinan, China). In order to create a hyperocclusive state 1 mm MEAW was bonded on the occlusion surface of the first molar at left upper jaw by means of super-bond composite resin accumulation to form the occlusal trauma model of BMS387032 the first molar at the same side of lower jaw, which was taken as the experiment group, whilst the lower jaw of the opposite side was taken as the contradistinctive group. After the treatment for 24 h, the animal was sacrificed by the intraperitoneal injection of chloral hydrate 40 ml/kg (Qilu Hospital), and then the first molars at the both sides of the lower jaw were extracted. Lower jaw bone tissues in the region of the extracted

teeth were ablated, isolated from the mandibles, placed in liquid nitrogen for immediate freezing, and stored in the −70 °C freezer. All the glassware and mortars

were baked at 200 °C for 4 h to inactivate RNA enzyme. The frozen alveolar bone was ground rapidly in liquid nitrogen. Trizol Reagent kit (Gibco BRL Company, USA) was used to extract total RNA of the tissues. Then used gel electrophoresis to test whether the extracted RNA SB-3CT was degradted, and measured the OD value (A260/A280) with spectrophotometer(Agilent, Shanghai, China) to test the content and purity of RNA. For gel electrophoresis the 28S and 18S ribosomal RNA bands should be fairly sharp, intense bands. The intensity of the upper band should be about twice that of the lower band, and for spectrophotometer, the O.D. A260/A280 ratio should be more than 1.8. The extracted RNA was stored at −70 °C. Microarray analysis was performed by rat genome-wide oligonucleotide microarrays in CapitalBio Corp. (Beijing, China).25 Briefly, a Rattus norvegicus genome oligonucleotide set (version 3.0),which was consisted of 269,625 amino acidmodified 70-mer probes representing 22,012 genes and 27,044 gene transcripts, was purchased (Operon, Huntsville, AL) and printed on silanized glass slides using a SmartArray™ microarrayer (CapitalBio). Five micrograms DNase-treated total RNA was prepared and fluorescent dye (Cy5 and Cy3-dCTP)-labelled cDNA, produced through Eberwine’s linear RNA amplification method26 and subsequent enzymatic reaction, were then hybridized to an array.

Since brain cytokine expression was comparable between FK565 and MDP, it appears unlikely that the FK565-evoked rise of plasma corticosterone was mediated by cytokines. Since nitric oxide (NO) participates in the activation of the HPA axis (Bugajski et al., 2004) and FK565 is more potent in inducing NO than MDP (Cartwright et al., 2007), NO may be a mediator of the cytokine-independent HPA axis stimulation due to NOD1 agonism. As MDP and FK565 were also unable to change body temperature, anxiety-like behavior and SP, we conclude that stimulation of NOD1 and NOD2 alone,

with doses of FK565 and MDP that enhance the effects of LPS, is insufficient to evoke an overt sickness response. Interaction and crosstalk between the signaling pathways of TLRs and NLRs lead to increased or decreased production HCS assay of proinflammatory cytokines, depending on the cell type tested (Elinav et al., 2011). Pretreatment of monocytic cells with NOD agonists can facilitate the LPS-induced production of various cytokines (Chamaillard et al., 2003, Fritz et

al., 2005, Park et al., 2007 and Uehara et al., 2005), and a similar synergistic increase of cytokine production following exposure to NLR and TLR agonists is seen in vivo ( Parant et al., 1995 and Shikama et al., 2011). Furthermore, priming with MDP enhances anaphylactoid reactions and lethality evoked by LPS ( Takada and Galanos, 1987 and Takada et al., 1990), while intravenous administration Kinase Inhibitor Library mouse of FK565 alone has been reported to elicit signs of septic shock in rats ( Cartwright et al., 2007). Priming with MDP can also aggravate the reduction of ingestion and locomotion induced by LPS in rats ( Engeland et al., 2003 and Langhans et al., 1990), whereas the behavioral effects of combined NOD1 and TLR4 agonism remained unexplored. The ability of NLR agonism to aggravate and prolong the sickness response to LPS is particularly highlighted by the LabMaster data. Specifically, the low dose of 0.1 mg/kg LPS was able to decrease only

locomotion and ingestion, while the combination of FK565 + LPS and MDP + LPS aggravated and prolonged the effects of TNF-alpha inhibitor LPS on all parameters tested (locomotion, exploration, ingestion, SP) and led to a significant decrease of locomotion, exploration (rearing) and food intake for 2–3 days. In contrast, SP was decreased for a shorter period of time. The LabMaster results also shed some light on the effect of single housing in immune–brain interactions. Housing conditions can modify affective behavior (Painsipp et al., 2011), and single housing made the animals more vulnerable by the PRR agonists. While, in line with the literature (Frenois et al., 2007), novelty-induced locomotion in the OF was not altered 1 day after treatment with 0.1 mg/kg LPS, home cage activity in the LabMaster was decreased for a longer period. Since avoidance of physical activity is a sensitive indicator of illness (Skinner et al.

This review and practice guide provides a comprehensive summary of the monogenic causes of IBD-like intestinal

inflammation and a conceptual framework for the diagnostic evaluation of patients with suspected monogenic IBD. We categorize mTOR inhibitor known genetic defects into functional subgroups and discuss key intestinal and extraintestinal findings. Based on the enrichment of known causative mutations as well as extreme phenotypes in very young children, we have focused on a practical approach to detect monogenic disorders in patients with VEOIBD and infantile IBD in particular. Because there is only modest biological evidence to support age-specific categorization of IBD above infantile IBD and within the EOIBD subgroup, we also discuss disease- and gene-specific ages of onset of intestinal inflammation (Figure 1). Approximately check details 20%

to 25% of patients with IBD develop intestinal inflammation during childhood and adolescence. IBD in children younger than 1 year of age has been reported in approximately 1% and VEOIBD in approximately 15% of pediatric patients with IBD.6 VEOIBD has an estimated incidence of 4.37 per 100,000 children and a prevalence of 14 per 100,000 children.22 The incidence of pediatric IBD is increasing.22 and 23 Some studies have reported that the incidence of IBD is increasing particularly rapidly in young children,24 and 25 although not all studies have confirmed this observation.9 Twin studies have provided the best evidence for a genetic predisposition to IBD,

which is stronger for CD than UC. Conventional IBD is a group of polygenic disorders in which hundred(s) of susceptibility loci contribute to the overall risk of disease. Meta-analyses of (genome-wide) association studies of adolescent- and adult-onset IBD identified 163 IBD-associated genetic loci encompassing approximately 300 potential candidate genes. However, it is important to consider that these 163 Mirabegron loci individually contribute only a small percentage of the expected heritability in IBD.26 This suggests that IBD, including CD and UC, can be regarded as a classic polygenic disorder. Findings from initial genome-wide pediatric association studies focused on adolescents and confirm a polygenic model.27 and 28 There are no well-powered genome-wide association studies of patients with EOIBD or VEOIBD. Although most cases of IBD are caused by a polygenic contribution toward genetic susceptibility, there is a diverse spectrum of rare genetic disorders that produce IBD-like intestinal inflammation.29 The genetic variants that cause these disorders have a large effect on gene function. However, these variants are so rare in allele frequency (many private mutations) that those genetic signals are not detected in genome-wide association studies of patients with IBD.

L. Ren Jenny Renaut Nicole Richoux Jan Rijstenbil Amy Ringwood F. Robledano Riccardo

Rodolfo-Metalpa G. Roesijadi Sergio Rossi G.L. Sanchez Gianluca Sarà N.S. Sarma J. Sarrazin Nicolas Savoye Felicita Scapini Doris Schiedek K.B. Schneider Michaela Schratzberger M.S. Sepulveda S. Shang Jenny Shaw Jian Shen K. Sherman Graham Sherwood P.V. Shirodkar Laura Sigg Stuart Simpson Annelie Skoog Vera Slavekova M. Smirnoff Akio Sohma Montserrat Sole Luis Soto Manu Soto M.F.L. Souza Alan Springer Annaamlai Subramanian Alex Sukhotin Teri Sutherland David Sutherland S. Taljaard Heather Tallis S. Trametinib in vitro Tanabe Antonio Terlizzi Jorge Terrados Johannes Teuchies Peter Thomas Richard Thompson M.F. Tognelli Moshe Tom Brant Touchette Ashley Townsend Clara Turetta Andrew Turner David Turner R.E. Turner Niklas Tysklind Wann Tzeng Richard Unsworth J.P. Valdes Herman

Van Leeuwen Jamie Vaudrey Aldo Viarengo Pierluigi Viaroli Vjercocka Vojvodic Terry Wade D. Wagner Wen Wang Wen Xiong Wang Wendy Wang Bess Ward Michel Warnau Michael Wetz Steve Widdicombe John Widdows Claudia Wiegand Steven Wilhelm Isaac Wirgin David Wright Rudolf Wu X. Xia Dawit Yemane Jennifer Yordy Jian-xin Zhao Izaskun Zorita Mikhail Zubkov Full-size table Table options View in workspace Download as CSV “
“A salient change trans-isomer cell line in a sound is likely to draw our attention to its location (Näätänen, 1992). Similarly, a salient change in prosody can trigger anticipatory attention to upcoming grammatical information ( Roll and Horne, 2011). An illustrative example is Central Swedish, where word stems with a high tone, e.g. lekH–‘game’ are followed by a certain class of suffixes including plural –ar, as in lekH–ar ‘games.’ Low stem tones are followed by another class of suffixes, including the singular definite morpheme –en as in lekL–en ‘the game’

( Fig. 1A). Since the choice of stem tone depends on which suffix is attached to the stem, suffixes can be referred to as ‘high tone-inducing’ (e.g. plural –ar) or ‘low tone-inducing’ (e.g. singular definite –en). The perception of Urease a rise to a high stem tone has previously been found to produce an increased P2 component at 200–300 ms after onset in event-related potentials (ERP) ( Roll et al., 2010). The positivity has been thought to indicate allocation of passive anticipatory attention to the tone-inducing suffixes ( Roll and Horne, 2011 and Roll et al., 2011b). High tone-inducing suffixes (e.g. plural –ar) not preceded by their required high stem tone accordingly produced a P600-like effect at 400 to 900 ms after their onset, indicating that they were unexpected.

Activity of putative matrix metalloproteinases 2 and 9 was detected with gelatin zymography. Ten ontogenetic and 10 regenerated zebrafish scales were cultured for 20 h in 100 μl MEMα (Invitrogen). Zymography was done according to Bildt and co-workers [48]. Relative MMP activity was calculated from band intensity with Quantity One software (Bio-Rad, Hercules, USA) and related to 2 ng human recombinant

FK228 purchase proMMP-2. GM6001 (ilomastat) from Millipore (Billerica, USA) was dissolved in DMSO at a concentration of 1 mg/ml. From two groups of six fish each, approximately 50 scales were removed from the left side of the fish. To specifically investigate MMP activity during scale plate remodelling, GM6001 exposure (100 nM) was started at day 2 in one group while the other group was exposed to the vehicle. Water was replaced every other day. On day 4 and day 7, three fish from each tank were sacrificed. Medium from overnight scale cultures was concentrated approximately fivefold by vacuum drying. Samples were loaded on a SDS-PAGE gel according to standard procedures. Proteins were transferred to an Immobilon-P PVDF membrane (Sigma-Aldrich) and used for Western blot with anti-MMP-9 (Anaspec) at a dilution of 1:1000. Biotinylated anti-rabbit IgG (Vector Laboratories, Burlingame, USA) was used as second antibody at a dilution of 1:1500. The Western

blot was developed with Vectastain ABC kit (Vector Laboratories) according to manufacturer’s instructions for staining with nickel-diaminobenzidine selleck kinase inhibitor (Ni-DAB). Twenty scales (ontogenetic or 6 days regenerating) were taken from 6 fish and cultured overnight Vildagliptin in 200 μl MEMα. Collected culture medium was mixed with 400 μl 100% ethanol and allowed to precipitate overnight. Samples were centrifuged 15 min at 1710 g and supernatants were collected. Pellets were washed with 200 μl 70% ethanol and supernatants

were added to previously obtained supernatants. Samples were dried in a hot stove and then resuspended in 50 μl 2 M NaOH. Samples were autoclaved for 30 min and hydroxyproline was measured according to the method described by Reddy and Enwemeka [49]. In ontogenetic (non-plucked) scales of adult male zebrafish, mmp-9 expression was confined to cells on the episquamal side, along the radii and margins of the scale (see Figs. 1A, B, and D for whole-mounts and Figs. 1C and E for histological sections). Scleroblasts on the hyposquamal side showed no hybridisation; the mmp-9-positive cell population was confined mainly to the episquamal surface of the scale and included both mononucleated cells ( Figs. 1C and D) and multinucleated cells ( Figs. 1B and E). Fig. 1F shows a superimposed confocal image of plasma membranes stained with concanavalin A FITC conjugate. No separate plasma membranes were seen dividing the cytoplasmic mass of cells similar to the mmp-9 expressing cell in Fig. 1B.

In the literature, a storm surge is variously defined, depending on the criteria adopted. The Encyclopaedia of Coastal Science (2005) defines a storm surge as an increase in ocean water level near the coast generated by a passing storm, above that resulting from astronomical tides. A different definition

is provided by the International Glossary of Hydrology (1992): here, a storm surge is an elevation of Epigenetics inhibitor the sea level caused by the passage of a low pressure centre. Gönnert et al. (2001) define a storm surge slightly differently, viewing it as oscillations of the water level within a coastal area and coastal water regions, lasting for several minutes to several days, resulting from the impact of pressure systems on the sea surface. The generation of a storm surge occurs Tyrosine Kinase Inhibitor Library either as a result of the impact of an extremely strong wind and decrease of atmospheric pressure at the sea surface (Weisse & von Storch 2010), or generally, only as a result of a strong wind (Jensen & Müller-Navara 2008). For the German coasts of the Baltic Sea, a storm surge is usually considered to be an increase in sea level of at least 100 cm above the mean level, that is,

600 cm Normal Null. The Polish coastal protection services describe a storm surge as a dynamic rise in sea level above the warning level (570 cm N.N., that is, 70 cm above mean level) and the alarm level (600 cm N.N.), induced by the action of wind and atmospheric pressure on the sea surface (Majewski et al. 1983). Wiśniewski (1997) considered a storm surge to be the dynamic increase of water level under the influence of wind and atmospheric pressure on the sea surface above the level of 570 cm on any section of the Polish coast (maximum storm surges greater than or equal to 70 cm NAP), associated with a temporary pressure system and wind causing the Carbohydrate difference in the sea surface elevation. This criterion was also referred to in the later works of Wiśniewski & Wolski (2009a), Wolski & Wiśniewski (2012); it is the one used in this study. On the south-western coasts of the Baltic Sea, the strongest surge recorded

since regular recording began occurred on 13 November 1872 (Majewski, 1998 and Richter et al., 2012). This surge was recorded in many ports on the western coast of the Baltic, even exceeding 3 m above mean level (3.31 m in Lübeck, 2.22 m in Kołobrzeg). The conditions of catastrophic surges on the German coasts of the Baltic have been studied by many scientists (Stigge, 1994, Hupfer et al., 2003 and Gurwell, 2008, Jensen & Müller-Navarra 2008, Rosenhagen and Bork, 2009 and Richter et al., 2012). In the Gulf of Finland, the highest surges occur in its eastern part, in the St. Petersburg region. On 19 November 1824, the sea level there reached 4.21 m above the mean sea level (Averkiev and Klevanny, 2007 and Averkiev and Klevanny, 2010). High surges have also been recorded on the coasts of the Gulf of Riga (Suursaar et al.

Continuous variables were shown as mean ± standard error, and the differences among each group were compared by Kruskal-Wallis one-way analysis of variance followed by Student t test. Categorical variables were analyzed by Fisher exact test. A P value of < .05 was considered statistically significant. Statistical analysis was performed with JMP 9.0 software (SAS Institute Inc, Cary, NC). Transgastric access to the peritoneal cavity was successfully created in all dogs with a mean time of 5.0 ± 0.4 minutes. Peritoneoscopy revealed no access-related damage to the adjacent organs

and abdominal wall. Gastrotomy closure was easily achieved in groups B, C, and BLZ945 supplier D, with a similar average procedure time (5.8 ± 0.4 minutes, 6.2 ± 0.4 minutes, and 6.3 ± 0.6 minutes, respectively). In contrast, closure by endoclips (group Galunisertib A) appeared to be more time-consuming, especially for the large, gaping defects, as shown by significantly longer closure time (35.4 ± 1.9 minutes) than the other 3 groups (Table 1,P < .001). Accordingly, more

clips were needed for the gastrotomy closure in group A (7.3 ± 0.5 clips) than in group B (3.0 ± 0.1 clips, P < .001). In group C, one OTSC clip was sufficient to close the gastric opening in each of the 10 cases. As shown in Table 1, the leakage tests using explanted stomachs revealed a mean leakage pressure of 81.5 ± 2.1 mm Hg in the OTSC closure group and 87.0 ± 3.0 mm Hg in the hand-suturing group, significantly higher than the omentoplasty group (42.2 ± 4.1 mm Hg) 17-DMAG (Alvespimycin) HCl or endoclip group (34.5 ± 2.6 mm Hg) (P < .001, analysis of variance). No statistical difference was found between the endoclip and OP groups (P = .09). During the follow-up period, 2 of 6 animals (33.3%) in group A had a high-grade fever fluctuating from 38.5°C to 41.0°C 24 hours after NOTES, accompanied by shivering, lethargy, and loss of appetite. The general condition of these two dogs was deteriorating, which was considered to be related to severe infectious

adverse events. At the discretion of the veterinarians, they were killed prematurely with euthanasia on day 7. At necropsy, the gastrotomy sites were found to be unsealed with spillage of gastric contents into the peritoneal cavity, together with purulent peritonitis and extensive adhesions (Fig. 3A, B). The cause of death was therefore deemed to be acute peritonitis secondary to gastric content leakage (Table 2). The remaining 18 animals survived over 2 weeks with no evident clinical symptoms or signs of illness. On day 14, a repeat endoscopy and necropsy after the dogs were killed were performed, revealing good healing and no gross abnormalities in all 18 surviving animals. Over half of the endoclips had dislodged in groups A and B, and the remnant clips were seen attached superficially, no deeper than the mucosal layer.

They provide proof-of-concept data for the treatment of apathy which is increasingly recognized to be a key component of several neurological disorders (Bonelli and Cummings, 2008;

Marin, 1991; Chow et al., 2009; Starkstein, 2009). Unlike other tasks involving risk, such as the Iowa Gambling Task (Bechara et al., 1994) or the Cambridge Gamble Task (Clark et al., 2004), our TLT requires participants to take risks by making anticipatory responses. Many other paradigms place certain and risky options on an equal footing with the same amount of effort required for both choices. This has the benefit of establishing risk preferences independently of effort but tends to favour a careful, deliberative response strategy. The traffic lights paradigm imposes time constraints on decisions

and rewards behaviour that might be considered ‘functionally JQ1 chemical structure impulsive’ (Dickman, 1990): on this task, it can be functionally useful to make anticipatory responses because these can lead to greater rewards, analogous to many situations in real life. It is possible that KD’s Lumacaftor lack of anticipatory responses on this task reflects risk aversion, rather than lack of motivation or unwillingness to make an effort for rewards. However, it is less easy to explain how such a mechanism might account for behaviour on the directional saccadic task, where there was no risk of incurring a penalty. How did dopamine reverse apathy and reward insensitivity? Substantial evidence links dopamine to reinforcement learning (Schultz, 2007). However a growing body of research also implicates dopamine in effort-based decision-making, generating the motivation and vigour to overcome costs of initiating actions (Niv et al., 2007; Kurniawan et al., 2011). The progressive improvement of KD’s performance on the TLT immediately post l-dopa (Fig. 6B) is suggestive of dopaminergic enhancement of learning. However, during the drug holiday period such learning was radically reversed (Fig. 6C), suggesting that if this effect

Forskolin was solely due to a reinforcement learning effect of l-dopa it had not been completely consolidated. Dopamine was still required to maintain it. On the directional reward-sensitivity task, l-dopa also had a dramatic effect after its introduction, speeding saccades to the RS (Fig. 7). During the drug holiday, however, there was no longer any significant reward-sensitivity but saccades were generally faster than before treatment, suggesting there were some general, non-specific effects of practice on the task. The time course of action on reward-sensitivity and its reversal during the drug holiday makes it unlikely that dopaminergic effects on synaptic plasticity and learning were the only mechanism of action. Instead, it might also have had an effect on response vigour or overcoming costs of effort (Niv et al., 2007; Kurniawan et al., 2011).

TN has received research grants and/or consulting fees (Asahi Kasei Pharma, Astellas, Banyu, Chugai, Daiichi Sankyo, Eisai, Eli Lilly Japan Ono, Takeda, Teijin Pharma); belongs to the Japan Ministry of Health, Welfare and Labor as a councilor for hospital administration and social medical insurance. MF has received a consulting fee (Astellas). MS has received consulting fees (Asahi Kasei Pharma, Astellas, Chugai, Daiichi Sankyo,

Teijin Pharma); lecture fees (Eisai, Ono). TM is a member of musculoskeletal global advisory board (Lilly); has received consulting fees (Asahi Kasei Pharma, Astellas, Chugai, Daiichi Sankyo, Eli Lilly Japan, JT, Ono, Teijin Pharma). We thank the doctors who participated in the clinical trial. This study was supported in part by a grant for the Promotion of Fundamental Studies in Health Sciences from the National Institute of Biomedical Innovation selleck chemicals llc (NIBIO) of Japan (06–31 to MI). “
“Vitamin D metabolism plays an essential role in regulation of mineral and bone homeostasis [1]. The active form of 1α,25-dihydroxyvitamin D3 (1α,25-(OH)2D3),

acts through the vitamin D receptor (VDR) present in target organs such as the intestines, kidney and parathyroid glands. It stimulates calcium absorption and reabsorption while blocking both the synthesis and secretion of another essential regulator of mineral balance, the parathyroid hormone (PTH) [2]. VDR has also been found in osteoblasts and osteoclasts, suggesting that vitamin D may directly affect the skeleton [3] and [4]. In bone, the hormone is MAPK Inhibitor Library screening important in at least two different ways: first, it interacts with the VDR in osteoblastic cells and regulates osteoclastic activity via the osteoprotegerin (OPG)/receptor activator nuclear factor kB (RANK)/RANK ligand (RANKL) system [5]; second, it secures a supersaturated state of calcium–phosphorus products in the blood, which indirectly enables osteoid mineralization [6]. Vitamin D deficiency may lead to exacerbated bone resorption as a result of increases in osteoclast number and activity, and may also cause a type of bone mineralization defect known as rickets in children and osteomalacia

in adults [7]. Interestingly, 1α,25-(OH)2D3 was shown to promote osteoclastic bone resorption in culture [8] and in vivo [9] and to enhance the expression of RANKL on bone marrow stromal cells Rho [10]. Despite its good acceptance in the management of conditions like psoriasis [11] and cancers [12], the use of vitamin D in the treatment of osteoporosis has been hindered due to its calcemic activity and the notion that the hormone drives osteoclastic bone resorption [13], [14] and [15]. However, there have been reports showing that the therapeutic effect of active vitamin D can be dissociated from the one on calcium absorption [16] and that it is mostly related to suppression of bone resorption due to decreases in the pool of osteoclast precursors [17] and [18].

Hence, at sites with more than 3 m of water, the bottom reflectance contributes nothing to Lwnred although the latter remains sensitive to resuspended bottom sediments penetrating the near-surface layer. In other words, the 3 m depth is a universal threshold of red radiance sensitivity to bottom reflection ( Figure 1), and the similarity of the horizontal distributions of Lwnred and Lwnref over the shallow area points to a particularly strong resuspension GW 572016 of bottom sediments, because Zor for Lwnref delimits a much thicker surface layer than Zor

for Lwnred does (Lwnref /Lwnred criterion). We chose a shallow in the south-eastern Caspian Sea as the study area (Figure 2) because it has the features of a desired natural model: (1) the waters of the South Caspian basin, flowing across the shallow, are fairly transparent (Simonov & Altman 1992), which facilitates observations of resuspension effects; (2) the bed of the shallow is mainly free of sea grass and consists of bare sand, silt and other light-coloured sediments that are detachable from the sea floor by quite moderate water motions; (3) digital bottom topography of the Caspian

Sea is available online at http://caspi.ru/HTML/025/02/Caspy-30-10.zip (Figure 2b); (4) the shallow extends for about 200 km in latitude and from 40–50 to 110–120 km in longitude and is clearly delimited Pictilisib purchase by the shore line in the east and by an underwater precipice to the west of the 20–30 m depth contours (Figure 2b); (5) only a few rivers with a minor discharge rate enter the south-eastern Caspian Sea, which minimizes the occurrence of externally supplied sediments; (6) the bottom relief is fairly smooth at sites of plausible sediment resuspension (depth range up to 15–20 m, Figure 2b); (7) the south-eastern Caspian Sea is a region where sunny weather prevails. Our approach implies the use of a long-term data set of the Sea-viewing Wide Field-of-view Sensor of (SeaWiFS), since it is equipped with a sun-glint avoidance facility. Use has been made of archived water-leaving radiance distributions at wavelengths 412, 443, 490, 510, 555 and 670 nm as standard

level L2 products with pixel size 1.1 × 1.1 km, collected during the NASA global ocean mission in the 1999–2004. The second data set involves the daily estimates of the near-water before-noon wind vectors obtained at 15′ spacing with the scatterometer QuickScat in 1999–2004 and available at http://poet.jpl.nasa.gov. We restricted ourselves to eight wind velocity directions with the following designations and mean azimuths φi: S-N, φ1 = 0°; SW-NE, φ2 = 45°; W-E, φ3 = 90°; NW-SE, φ4 = 135°; N-S, φ5 = 180°; NE-SW, φ6 = 225°; E-W, φ7 = 270°; SE-NW, φ8 = 315°. Any wind vector in the range φi ± 22°30′ was assigned to the i-th direction. The SeaWiFS and QuickScat data and the bottom bathymetry were displayed for every year day (YD) as superimposed maps of the testing area (Figure 2).