Daneben führt die orale Einnahme von Eisen zu einer harmlosen Schwarzfärbung

des Stuhls. Im vorderen Dünndarm stehen die gesundheitsschädigenden Wirkungen in direktem Zusammenhang mit der eingenommenen Eisendosis [133]. Effekte im Kolon korrelieren weniger gut mit der eingenommenen Dosis, da Unterschiede hinsichtlich der Resorption, der Darmpassagezeit und der Bindung an Nahrungsmittelliganden die Verfügbarkeit der Eisenionen beeinflussen. Nichtsdestoweniger sind die Daten hinsichtlich eines Zusammenhangs Epigenetics Compound Library mw zwischen eingenommenen Eisendosen und eisenvermitteltem oxidativem Stress im Kolon sowie dessen vermutetem Einfluss auf lokale Entzündungen und Karzinogenese weniger widersprüchlich als bei anderen Organen, wo die lokale Verfügbarkeit des Eisens durch zusätzliche homöostatische Mechanismen beeinflusst wird (siehe Abschnitt „Eisenhomöostase this website und das Potenzial des Eisens für schädliche Auswirkungen”). Die soliden Daten zur Dosis-Wirkungs-Beziehung für die eisenabhängige Erosion und Irritation der Schleimhaut im Darmbereich haben

das US-FNB [73] veranlasst, auf dieser Grundlage eine Obergrenze für die sichere Eisenaufnahme mit der Nahrung abzuleiten. Die gesundheitsschädigende Wirkung hängt ab von den Konzentrationen an freiem Eisen im Lumen. Sie sind am höchsten, wenn Eisenpräparate auf nüchternen Magen eingenommen werden, und nicht von Eisenliganden in der Nahrung beeinflusst werden Inositol monophosphatase 1 (siehe Abschnitt „Die Grundlagen für Empfehlungen zur Eisenaufnahme”). Daher sind die Irritation und Erosion der Mucosa durch labile Eisenionen nach der Einnahme pharmakologischer Dosen von Eisenpräparaten auf nüchternen Magen kein realistisches Szenario, um das Risiko bei der Aufnahme von Eisen mit der Nahrung bei niedrigeren Konzentrationen und in der Gegenwart von Nahrungsmittelliganden zu beurteilen [136]. Nach Verabreichung von 80 mg Eisen über eine Magensonde erhöhte sich die TBARS-Konzentration im Lumen des Zwölffingerdarms freiwilliger menschlicher Probanden innerhalb von 30 Minuten

deutlich. Dies deutet auf eine oxidative Schädigung im Darmlumen [137], die mit einem signifikanten Anstieg der antioxidativen Kapazität (in Troloxäquivalenten), Veränderungen der Expression von Genen für G-Protein-Rezeptor-gekoppelte Signalwege, Komplementaktivierung und Störungen des Zellzyklus [138] einhergeht und zu den direkten gastrointestinalen Nebenwirkungen oraler Eisenpräparate hinzukommt. Zwei Wochen Supplementierung menschlicher Freiwilliger mit 19 mg Fe/Tag erhöhte die Konzentration des verfügbaren Eisens in den Faeces von 60 auf 300 mmol Fe/L und steigerte die Produktion freier Radikale signifikant um 40%; es wird angenommen, dass es hierdurch zur Karzinogenaktivierung aus Vorläufern in der Nahrung kommt [139].

The border-line Rivers are #3 and #10 for which the confidence limits are ±0.29, ±0.27 and therefore their respective sample estimates of 0.28 and 0.26 for ρ1 are found to be well contained within the confidence limits. So for the purpose of hydrologic drought analysis, the annual SHI sequences of rivers considered in this paper selleck screening library are regarded to be independent normal sequences. For each river, the values of statistics μ, σ or cv and γ of monthly flow series were computed ( Table 2) and necessary plots were prepared

in terms of the product moments and L-moments. The scatter of points (γ against cv) in the product moment ratio diagram ( Fig. 2A) is a good indicator of the probability distribution of monthly flows to be Gamma rather than Lognormal OTX015 datasheet pdf. To affirm the hypothesis of the Gamma distribution, the L-moments were computed for the Gamma pdf and the plot of L-skewness (τ−3) versus L-kurtosis (τ−4) ( Vogel and Fennessey, 1993) was drawn. The L-moment plot (L-kurtosis versus

L-skewness) exhibits a good correspondence between the observed and the Gamma distributed points ( Fig. 2B) thus affirming the hypothesis that the Gamma pdf is a reasonable descriptor of the monthly flow series for rivers under consideration. It is to be noted that 12 sets of cv and γ values were averaged-out (designated as cvav and γav (where, γav represents the average value of 12 values of cross correlations between adjoining months. That is, the cross correlation between January–February, February–March, and so

on (as summarized in Table 2) for plotting purposes and they also proved to be a better estimator of the drought duration, E(LT) and magnitude, E(MT). Once the underlying probability distribution of monthly flows was chosen, the next step was to identify the dependence structure in the SHI sequences using lag-1 autocorrelation (ρ1). The computed values Niclosamide of ρ1 were found to be significant ( Table 2), which alludes to that monthly SHI sequences possess dependence structure. Furthermore, the autocorrelation function of the SHI sequences ( Box and Jenkins, 1976) was found to mimic the process of an autoregressive order one (AR-1). The diagnostic checks based on the Portmanteau statistics (computed from first 25 values of autocorrelations of the residuals in the SHI sequences after fitting AR-1 model) further affirmed the Markovian dependence. In succinct terms, the monthly SHI sequences possess the first order dependence implying that a drought length model must contain terms to account for such dependence. Based on the foregoing analysis, the extreme number theorem and the Markov chain-1 models can be considered as potential models to capture the first order dependence structure in monthly SHI sequences. For identification of the pdf of weekly flow series, the same procedure used for monthly flows was adopted.

Statistical analysis was performed using SPSS version 16.0 statistical software (SPSS, Inc., Chicago, IL). χ2, t, and Fisher’s exact tests were used when appropriate. A biostatistician who was blinded to the study groups performed the statistical analysis. We enrolled to this study, 363 children aged more than 5 years with major thalassemia (169 boys, 194 girls) who were receiving blood as the patient group and 363 children without thalassemia aged 4–7 years (154 boys, 209 girls) who had referred to healthcare centers for routine health monitoring as the control group. Of the 363

patients with thalassemia major, 4 patients were excluded from the study because of psychomotor retardation (PMR), suspected shivering, suspected breath holding, and history of convulsion at the age of 10 months and long hospital stay. In the control group, 6 children were excluded for reasons such as having meningitis (n = 1), shigellosis (n = 2), and suspected shivering Vorinostat (n = 3). Among the children with thalassemia major,

4/359 (1.1%) had a history of febrile convulsion see more as compared with 14/357 (3.9%) children in the control group (P = 0.017, χ2 test). Among the four children in the case group who had a history of febrile convulsion, 3 (1.8%) were girls and 1 (0.5%) was a boy (P = 0.25), compared to 9 (5.8%) boys and 5 (2.4%) girls in the control group (P = 0.09). In overall, 18 children had a history of febrile convulsion in both groups including 12 (66.7%) boys and 6 (33.3%) girls.

The mean (±SD) age of the initial onset of febrile convulsion in both groups was 20.26 (±9.1) months (range: 6–36 months). The mean (±SD) age of the initial onset of febrile convulsion in the case and control groups were 22.5 (±12.4) and 19.7 (±8.4) months, respectively (P = 0.59, t test). Of the 4 children who had experienced febrile convulsion in the case group, 3 (75%) had experienced the simple type of febrile convulsion while Doxacurium chloride 1 (25%) had experienced the complex type. In the control group, 11 (78.6%) children had had the simple febrile convulsion, while 3 (21.4%) had had the complex type (P = 0.99, Fisher’s exact test). According to existing evidence, the complex balance between the activities of the glutamate-GABA systems plays an important role in controlling convulsions. Iron deficiency probably reduces the activity of GABA systems leading to the occurrence of convulsion [7]. Therefore, Iron overload may reduce the incidence of convulsion by increasing the activity of the GABA system which is an inhibitory neurotransmitter in the brain. Our results show that the occurrence of convulsion was significantly lower in patients with thalassemia major (1.1% vs. 3.9% in the case and control groups, respectively) and this finding further suggests that children with thalassemia major may have increased serum iron levels and such increased serum iron levels may has a protective role against febrile convulsions.

30 According to the present study, elevated circulating levels of pro-inflammatory TSA HDAC research buy cytokines such as TNF-α and IL-6 released during experimental ligature-induced PD could possibly inhibit CeA-projecting neurons that block facilitatory mechanisms

present in the CeA and reduce the cardiovascular, dipsogenic and natriorexigenic effects of muscimol injected into the LPBN. We do not exclude the possibility of participation by other pro-inflammatory cytokines such as IL-1β and IL-8 in the reduction of water and hypertonic NaCl intake induced by muscimol injected into the LPBN in rats with experimental ligature-induced PD. This is not surprising given the several mediators activated by PD.7 The precise mechanism through which ligature-induced PD inhibits the dipsogenic and natriorexigenic

effects of muscimol was not addressed in the present study. A hypothesis is that pro-inflammatory cytokines may modulate GABAergic neurotransmission.14, 15 and 31 For example, administration of IL-1β and IL-6 reduced the frequency of sIPSCs and GABA-induced currents in dorsal horn neurons14 and amygdala neurons.15 Another hypothesis to explain the present results is that the cytokines TNF-α and IL-6 released during ligature-induced PD reduce the Rutecarpine levels of endogenous selleck inhibitor angiotensin

II (ANG II) in the LPBN. Recently, we showed that pre-treatment of the LPBN with injections of the nonapeptide angiotensin II receptor type 1 (AT1) receptor antagonist losartan reduced the dipsogenic and natriorexigenic effect of muscimol injected into the same site in fluid-replete rats and FURO + CAP-treated rats, suggesting that deactivation of LPBN inhibitory mechanisms by muscimol is facilitated by endogenous ANG II acting on AT1 receptors in the LPBN, which drives the rats to ingest large amounts of hypertonic NaCl.32 Therefore, ANG II acting on AT1 receptors in the LPBN facilitates the effects of muscimol injected into the LPBN on water and sodium intake.32 It is possible that the pro-inflammatory cytokines TNF-α and IL-6 released during PD reduced the effect of ANG II on AT1 receptors in the LPBN and inhibited water and sodium intake produced by muscimol in the LPBN. Although feasible, using these hypotheses to explain the effects of muscimol injected into the LPBN in rats with periodontal disease still has to be tested.

A value of p < 0.05 was considered statistically significant. Figures were obtained by the Statistical Analysis System (GraphPad Prism 4, GraphPad Software Inc., USA). Before

antidepressant fluoxetine treatment, we established rat animal model of anhedonia induced by CUMS procedure for the evaluation of the effectiveness of depression. As reported previously by us and others (Pan et al., 2010, Pan et al., 2013, Willner, 1997 and Willner et al., 1987), 6-week CUMS procedure caused anhedonia behavior (measured as a reduction of sucrose solution intake, −27.4%, p < 0.001) with significant decrease of body weight gain (p < 0.01) compared with Non-CUMS rats ( Fig. 1). During 6-week of fluoxetine treatment, the effect of CUMS procedure on rat anhedonia behavior (Week 12, p < 0.001) and body weight reduction (Week 12, p < 0.001) maintained or aggravated over time compared Epigenetics inhibitor with Non-CUMS group. Fluoxetine treatment significantly ameliorated this anhedonia in CUMS rats (Week 12, p < 0.001), without effect on body weight. In this study, IL-1β concentrations in serum were slightly but non-significantly increased in rats compared with Non-CUMS group, without the detected change of IL-1β concentrations Selleck Ivacaftor in CSF after 12-week CUMS procedure (Fig. 2A). Whereas, PFC IL-1β mRNA (Fig. 2B) (p < 0.01) and protein ( Fig. 2C and D) (31 and 17 kDa, p < 0.001) levels were significantly increased in CUMS rats compared

with Non-CUMS group. Interestingly, the promoted maturation

of PFC IL-1β was observed in CUMS rats ( Fig. 2C and D). These results suggest CNS-derived IL-1β as a sensitive inflammatory molecule in this animal model of depression. IL-1β abnormal expression in PFC including post-transcriptional regulation may be involved in the pathological mechanism of CNS inflammation in depression. Fluoxetine treatment for 6 weeks remarkably decreased PFC levels of IL-1β mRNA (p < 0.01), pro-protein (31 kDa, p < 0.001) and mature-protein (17 kDa, p < 0.01) in CUMS rats, without change of IL-1β concentrations in both serum and CSF. To explore whether the regulators were involved in CUMS-induced IL-1β expression alteration, we analyzed the phosphorylation levels of NF-κB, IKKα and triclocarban IKKβ in PFC of CUMS rats. CUMS procedure remarkably up-regulated p-NF-κB, p-IKKα and p-IKKβ levels (p < 0.001) in PFC of CUMS rats compared with Non-CUMS group ( Fig. 3A–D). These data demonstrate PFC NF-κB pathway activation, being consistent with up-regulation of PFC IL-1β mRNA and protein levels in CUMS rats. 6-week of fluoxetine treatment significantly inhibited CUMS-induced PFC NF-κB pathway activation (p-NF-κB, p < 0.001; p-IKKα, p < 0.01; p-IKKβ, p < 0.01) in rats ( Fig. 3A–D), suggesting that suppression of PFC NF-κB inflammatory pathway is involved in the antidepressant effect of fluoxetine in this animal model. Next, we analyzed the expression of PFC NLRP3 inflammasome components in CUMS-induced PFC IL-1β alteration of rats.

Time to death in the remaining patients ranged from 3.3 to 28 months. None of the patients that presented with local disease only went on to develop visceral metastatic

disease. Results demonstrate that the “first in man” EUS-FNI of www.selleckchem.com/products/incb28060.html recombinant poxvirus for treatment of pancreatic adenocarcinoma was well tolerated with the complete regimen suggesting an encouraging period of stable disease. While not powered to demonstrate a clinical effect, the results suggest a prolongation in survival of patients without preexisting metastatic disease, with none of these patients going on to develop metastatic disease. If these results were maintained in a larger Phase 2 study, it would be consistent with the generation of an endoscopically delivered tumor-specific immune therapy with anti metastatic activity. This study is supported by the NCI Cancer Therapeutics Evaluation Program (CTEP) and by NCI U01-CA07031 and P30-CA72720. “
“Endoscopic Ultrasound guided Radiofrequency Ablation (EUS-RFA) of pancreatic cystic neoplasms and neuroendocrine tumors (NET) have been previously described. The aim of this report is to outline the feasibility, safety, complications and early results of EUS-RFA in pancreatic neoplasms using a novel probe. Eight patients underwent EUS-RFA of a neoplastic

lesion in the head of the pancreas. A novel monopolar radiofrequency (RF) catheter (1.2mm Habib EUS-RFA catheter, Emcision Ltd, London) was placed through a 19 or 22 gauge fine needle aspiration (FNA) needle after FNA was performed. Angiogenesis chemical Eight patients [median age of 65 (range 27 - 82) years and 7 female and 1 male] were recruited in a prospective multicenter trial. Six had a pancreatic cystic neoplasm (four a mucinous cyst, one had IPMN and one a microcystic adenoma) and two had a NET in the head of pancreas (previously documented with diagnostic FNA cytology triclocarban and not suitable for surgical intervention). The mean size of the cystic neoplasm and NET were 36.5mm (SD +/−17.9mm) and 27.5mm (SD +/−17.7mm) respectively. RF (Rita or Erbe generator)

was applied at 5 watts, 15 watts, 20 watts and finally 25 watts in 3, 2, 2 and one patients respectively over 90 sec for each watt setting. The median number of applications were 4.5 (range 2 – 7). Patients with a cystic neoplasm and one patient with NET had one session of RFA each, whilst a second patient with NET had two sessions of RFA. The EUS-RFA was completed in all patients. Amongst the 6 patients with a cystic neoplasm, the post procedure imaging in 3-6 months showed complete resolution of the cysts in 2 patients, whilst in 3 patients there was 48.4% reduction [mean pre RF 38.8mm (SD +/−21.7mm) vs. mean post RF 20mm (SD +/−17.1mm)] in size. Using cross sectional imaging in 2 patients with NET, a change in vascularity and central necrosis after EUS-RFA was demonstrated. There were no episodes of pancreatitis, perforation or bleeding within 48 hours of the procedure.

In short, R-spondin-1 (enhances Wnt signaling), EGF (mitogen), Noggin (inhibits BMP signaling), and Matrigel (basement membrane substitute) are indispensable stem cell maintenance factors for small intestinal cultures find more with supplementary Wnt being necessary for colonic organoid growth. Human intestinal organoids additionally require nicotinamide, A83-01 (Alk inhibitor), SB202190 (p38 inhibitor), and prostaglandin E2 (PGE2, mitogen) for long-term expansion (human intestinal stem cell culture (HISC) condition). Differentiation can be achieved by withdrawing growth factors while simultaneously blocking Notch signaling (dibenzazepine, γ-secretase

inhibitor) [23•• and 24•]. Intestinal organoids are currently unique, because they efficiently form, self-renew, and expand long-term while remaining genetically stable [23••]. These features allow many applications ranging from basic to translational research [26 and 27]. Importantly, patient derived intestinal organoids emulate human disease as has recently been demonstrated

for cystic fibrosis [28•]. Currently, organoids are being established from a variety of tumors with colorectal cancer (CRC) leading the way. Cancer occurs through a chain of cellular alterations allowing uncontrolled proliferation and gradual loss of differentiation [29 and 30]. Most CRCs progress sequentially from adenomatous polyps to advanced adenomas, carcinomas in situ, and adenocarcinomas. There are strong indications that successive genetic changes are causal Veliparib order to cancer progression [ 31 and 32]. Mutations in the tumor suppressor gene

APC (adenomatous polyposis coli) or other Wnt pathway components (AXIN2, CTNNB1) can be found in most Quinapyramine microscopic lesions and are therefore considered initiating and rate-limiting mutations for the majority of CRCs [ 31 and 32]. Additional mutations associated with CRC affect DNA repair (MLH1, MSH2, and MSH6), cell-cycle regulation (TP53), and growth factor signaling (TGFBR2, SMAD4, KRAS, BRAF, and PTEN) [ 31 and 32]. Recent evidence furthermore suggests that cancer stem cells rather than random cells fuel tumor growth in several tissues including the intestine [ 33, 34 and 35]. It is therefore plausible to attempt culturing epithelial-derived cancers using the HISC protocol described earlier. Organoids are indeed readily established from surgically resected intestinal tissue and endoscopic biopsies of patients suffering from adenomas and adenocarcinomas [23••]. These CRC organoids grow as irregular compact structures and can be expanded seemingly indefinitely. Apart from Goblet and enteroendocrine cells, they mostly contain proliferating cells [23••]. The presence of differentiated cells within CRC organoids potentially allows conferment of drug resistance to cancer stem cells [36].

Because of this, it is suggested here that DPSIR should perhaps more accurately become DAPSI(W)R. In order to control those State changes and Impacts (or Impacts on human Welfare), we therefore require Responses. Those Responses may include bringing in technological advances (such as better

fishing gear, habitat re-creation or water treatment plants), economic instruments (such as quotas or penalties) or laws administered by statutory bodies. Hence we need a management framework to accommodate and describe all the linked processes in this framework. Such a framework must then be aimed at what we may term the ‘big idea’ – ‘that marine management is designed to protect and enhance the natural VX-770 mouse structure and functioning of the seas while at the same time ensuring the marine processes which deliver ecosystem services from which we then obtain societal goods and benefits’ ( Elliott,

2011). Hence many of the Impacts in Table 1 relate to a loss of ecosystem services this website and societal benefits. Given the adage that ‘if you don’t know where you are going then any road will take you there’, then in order to set down the ultimate aim as a readily communicable message, this should be encapsulated in a vision for the seas, for example to achieve ‘clean, healthy, safe, productive and biologically diverse oceans and seas’ as adopted by the UK government and others ( Defra 2010). Furthermore, it is argued that sustainable and successful marine management can then only be obtained by including all facets and players in the system, the so-called 10-tenets ( Elliott, 2013) in which the major players and responses are included. The latter suggest that our actions should be: Ecologically sustainable (identified as ecol. in the figures below), Technologically feasible (Tech.), Economically viable (Econ.), Socially desirable/tolerable (Soc.), Legally

permissible (Leg.), Administratively achievable (Admin.), Politically expedient (Pol.), Ethically defensible (morally correct) (Ethic.), Culturally inclusive (Cult.) and Effectively communicable (Comm.). This discussion and its diagrams will therefore try to indicate the major steps in an integrated marine management framework while cross-referring to the elements D, P, S, I(W) and R and the Farnesyltransferase 10-tenets. The Pressures on the marine environment (e.g. Kennish and Elliott, 2011) can be regarded as coming from three sources – activities which remove materials and space from the system, activities which place materials into the system, and thirdly, external and wider pressures, such as global climate change, which emanate from outside the system (Fig. 1). The materials extracted include fish, shellfish, water, and seabed sands and gravels, and space is also removed, for example by occupying the seabed with harbours, windfarms, etc.

5–16% combined (Bourne et Selleck BMS 777607 al., 2013). In Australia specifically, a 2005 study

found age-related macular degeneration (48%), glaucoma (14%), cataract (12%) and diabetic retinopathy (11%) to be the most common causes of blindness, with neuro-ophthalmic conditions accounting for an additional 3% of cases (Taylor et al., 2005). There were an estimated 530,000 vision impaired people in Australia as of 2004, including 50,600 who were categorized as legally blind (visual acuity of ≤6/60). This figure is predicted to rise as a result of population ageing; Taylor et al., 2005 and Taylor et al., 2006 estimated that approximately 70,000 Australians would be legally blind by 2014, and almost 90,000 by 2024 (Taylor et al., 2005 and Taylor et al., 2006). Moreover, increasing rates of obesity-related Type II diabetes (Shaw et al., 2010) will undoubtedly contribute further to these figures. The direct health system costs in Australia for age-related macular degeneration, glaucoma and cataract alone were A$490 million in 2004. Indirect financial costs relating to lost income and carer costs for all visual impairment were estimated at A$3.2 billion, exclusive of transfer costs including lost tax revenue and the expenditure related to carer

and welfare payments, which were estimated at A$850 million (Taylor et al., 2006). Visual impairment has been associated with a 2.3 fold increase in mortality (McCarty et al., 2001) and the costs specific to loss of well-being due Temsirolimus nmr to the impact of disease and premature mortality have been estimated using daily adjusted life years (DALY) at A$4.8

billion (Taylor et al., 2006). While medroxyprogesterone not a major focus of this review, biological therapies represent a promising suite of existing and emerging therapeutic options for blindness caused by retinal disease. Gene replacement therapy (McClements and MacLaren, 2013 and Petrs-Silva and Linden, 2014), modulation of ocular autoimmune responses (Ambati et al., 2013, Buschini et al., 2011 and Rieck, 2013), transplantation of stem cells, photoreceptor precursor cells or bioengineered sheets of retinal tissue (Barber et al., 2013, Fernandez-Robredo et al., 2014 and Pearson, 2014) plus intraocular administration of neurotrophic, anti-angiogenic, intraocular pressure-lowering and antioxidant agents (Zarbin et al., 2013) are all techniques that are either currently in use, at clinical trial stage or being investigated in the laboratory. Among the rehabilitative options available to the blind, sensory substitution is a concept that has been explored extensively. Sensory substitution operates on the principle of replacing input from a lost sensory organ with an artificial sensor, with the output of that sensor redirected to the input of one or more remaining senses. A simple example of sensory substitution is the mobility cane, wherein a representation of the blind user׳s physical environment is obtained via a tactile method (Bach-y-Rita and Kercel, 2003).

The nodes and arcs linking impact scenario variables to damage extent variables constitutes the second submodel of the BN, denoted GII(XII, AII). Its construction is described in Section 5. The integration of the two submodels GI(XI, AI) and GII(XII, AII) through the common variables leads to the final BN linking impact scenarios with oil outflow. The presented framework is generic in the sense that other, potentially more accurate, models could be used as underlying building blocks for the BN construction. The discussion on model validity in Section 7 is given as guidance on which parts of the model

would benefit most for reducing uncertainties and biases. However, the two main submodels (oil outflow conditional to damage extent and ship particulars and damage extent conditional to impact conditions) will inevitably be present in some form. www.selleckchem.com/products/EX-527.html Fulvestrant mouse The following sections show the model construction for a selected set of underlying models and assumptions. This Section describes the construction of the BN-submodel linking the oil outflow with variables describing the ship size and damage extent. The available data concerning tank configuration, the procedure for determining tank arrangement,

the calculation of oil outflow given a damage extent and the algorithm to learn the BN-submodel are described. The available data set containing tank configuration parameters consists of 219 product tanker designs which http://www.selleck.co.jp/products/Gemcitabine(Gemzar).html operate in the Baltic Sea.

These 219 tankers were selected based on their occurrence frequency in the Gulf of Finland: data was obtained from a ship database (IHS Maritime, 2013) for those tankers which enter the area at least twice during the year 2010. It is assumed that these frequently occurring vessels are representative of the entire product tanker fleet in the given area. The available tanker data is summarized in Fig. 3. The scatterplots above and below the diagonal show the relation between each two pair of variables, whereas the histograms on the diagonal provide insight in the relative number of occurrences of each class within a variable. For example, the histogram of TT shows that the vast majority (93%) of product tankers in the area have tank type 2, much fewer (5%) tank type 3 and only a small number (2%) tank type 1. The broadly linear relationship between L and B and the approximate third power relation between L and Displ are as expected. The relation between L and TT shows that TT2 configurations are found across the range of vessel lengths, whereas TT1 and TT3 are more often found in medium size product tanker vessels. The number of side tanks (ST) ranges from 4 to 10, with no apparent relation to the ship length.