A three-pool model which consists of water, the labile protons of interest and MT may be the

minimum required to model the in vivo environment. However, the z-spectra acquired at 7 T reveal a broad group of resonances between 0 and 5 ppm, and appreciable saturation Cabozantinib order effects observed between 0 and −5 ppm [29]. Thus, it is possible that a three-pool exchange model would be insufficient to perform the quantitative model-based analysis on a full z-spectrum. Having multiple pools in the model-based analysis is a challenging task even when the AP continuous approximation is used because the computational cost of matrix exponential in the analytical solution increases exponentially with the number of pools. Furthermore, increasing the number of pools in the analysis requires that more parameters have to be fitted from the data, leading to higher risk of

over-fitting and thus inaccurate results. The OSS discussed above may be one possible solution, since by selectively saturating Palbociclib certain frequency offsets, the contaminations from other labile pools can be avoided. Other simplified analytical approximations to the model solutions such as the relationship in [19] could also be considered, assuming that the inaccuracies introduced by the simplification can be acceptably accounted for. It is believed that the applicability of this study will still hold if the in vivo environment can be modeled accurately for slow exchanging protons. Studies on tissue-like phantoms with slow exchanging protons saturated by a series of short Gaussian pulses show no significant difference for the important fitted model parameters such as water center frequency shift and amine proton exchange rate when quantitative model-based analysis using either average power

approximation or discretization method is used. This suggests that when APT imaging is performed using a pulsed saturation with certain pulsed parameters, the fast continuous approximation (average power) to the time dependent RF irradiation pulses Oxalosuccinic acid can replace the computationally expensive discretization approach for quantitative model-based analysis. The authors would like to thank Dr. Heiko Schiffter for the help in preparing the pH phantoms. YT is funded by Qualcomm Scholarship from Qualcomm Inc. MAC is employed by The Centre of Excellence in Personalized Healthcare funded by the Wellcome Trust and EPSRC under Grant Number WT088877/Z/09/Z. AAK and NRS are funded by Cancer Research UK under Grant C5255/A12678. “
“The authors regret to have noticed that the numbering of the methyl groups 8 and 9 in the structure of isopinocampheol was interchanged in the initial Scheme 1. The corrected Scheme 1 can be found below. “
“NMR noise spectra, i.e. spectra obtained without rf-excitation of the observed nuclear spins, have recently attracted renewed interest both because of their fundamental aspects (e.g.

Total RNA was extracted with Trizol (Invitrogen) following manufacturer’s instructions. 2–5 μg of total RNA was DNase treated (Ambion, Inc., Austin, TX) and converted to cDNA by the High Capacity cDNA Archive Kit (Applied Biosystems, Foster City, CA). PCR was performed in 96-well plates. Both Assays-on-Demand Gene Expression Taqman primers (Applied Biosystems) and validated Syber Green primers (http://pga.mgh.harvard.edu/primerbank) were used for PCR. Glyceraldehyde-3-phosphate dehydrogenase (GAPDH) or β-actin served as endogenous control. All primers were checked check details for equal efficiency over a range of target gene concentrations.

Each sample was amplified in duplicate. PCR reaction mixture was run in Applied Biosystems Prism 7300 Sequence Detection selleck chemical System instrument utilizing universal thermal cycling parameters. Data analysis

was done using relative quantification (RQ, ΔΔCt) or the relative standard curve method. For alkaline phosphatase (ALP) staining, cells were fixed and stained with an alkaline phosphatase kit (Sigma) using the manufacturer’s instructions. Dishes were air dried and scanned into the computer. To assess mineralization, cells were washed with PBS, fixed in 100% V/V methanol on ice for 30 min and stained with 40 mM alizarin red-S pH 4.2 for 10 min at room temperature. Dishes were washed with water, air dried and scanned into the computer. For tartrate resistant acid phosphatase (TRAP) staining, cells were fixed with 2.5% glutaraldehyde in PBS for 30 min at room temperature and stained by the Leukocyte Acid Phosphatase Kit (Sigma) following company’s instructions. BMSCs were cultured for 14 days under similar conditions used for OB differentiation but without phosphoascorbate and β-glycerophosphate in the culture medium. Instead, 1 μM of insulin was added to the medium on day 7 to induce formation of fat bodies. For staining, cells were washed twice with 1× PBS, fixed with 4% paraformaldehyde

for 15 min at room temperature, rinsed with water and then incubated with oil red O working solution (3 parts to 2 parts water) for 1 h at room temperature. Dishes were washed with water, air dried and scanned into the computer. Media were over removed from cultured cells and frozen until assay. PGE2 accumulation was measured using an enzyme immunoassay (correlate-EIA™) kit following the manufacturer’s instructions (Assay Designs, Ann Arbor, MI). Confluent POBs were treated with 3 parts CM and 1 part of OB differentiation medium containing 0.5 mM isobutyl methyl xanthine (IBMX) 1 h prior to adding PTH or PGE2 for 20 min. Cells were scraped off in 400 μl/well of ice-cold ethanol. The ethanolic cell suspension was collected in tubes and centrifuged at 1500 ×g for 10 min at 4 °C. Supernatants were collected and evaporated to dryness using a lyophilizer. cAMP was measured using an enzyme immunoassay kit (Cayman Chemical, Ann Arbor, MI).

Finally, the ImpNon scale examines impulsive, antisocial and eccentric forms of behaviour (Cochrane et al., 2010 and Mason and Claridge, 2006). A 2 (Group) × 4 (Schizotypal Factor) mixed ANOVA was used to explore differences on each component of schizotypy between the groups.

A main effect of group was observed [F(1, 58) = 7.49, p = <.01], with synaesthetes scoring higher overall compared to controls. There was also a significant interaction [F(3, 174) = 3.37, p = <.05]. Bonferroni corrected post-hoc t-tests revealed that this was because synaesthetes showed significantly higher levels of positive (UnEx) [t(58) = 2.58, p = <.05, d = .68] and disorganised schizotypy (CogDis) [t(58) = 2.65, p = <.05, d = .70] relative to the matched control group ( Fig. 1A). No significant differences were found between the groups Selleck Ipilimumab in their levels of negative schizotypy (IntAn) [t(58) = .289, p = n.s, d = .08] or their ImpNon ( Fig. 1A) [t(58) = 1.53, p = n.s, d = .40]. Synaesthetes and controls also showed

significant positive correlations between UnEx scores and CogDis scores (synaesthetes: r = .490, p = <.01; controls: r = .486, p = <.01). Synaesthetes, but not controls, showed a significant positive correlation between UnEx scores AZD6244 research buy and ImpNon scores (r = .367, p = <.05). These findings show that synaesthesia for colour is linked to

an increase in positive and disorganized schizotypy, implying that the presence of synaesthesia is associated with widespread differences in cognition that extend beyond the synaesthetic experience itself. There are at least two potential mechanisms that may contribute to this effect: (i) the effect is modulated by co morbidity between synaesthesia and Clomifene other cognitive traits that are related to schizotypy; (ii) there maybe similarities in the underlying mechanisms that give rise to the perceptual reports associated with schizotypy and synaesthesia. In relation to cognitive traits, previous findings have linked heightened positive schizotypy to creativity (Nelson and Rawlings, 2010) and mental imagery vividness (Oertel et al., 2009). Synaesthesia has also been linked to higher levels of these cognitive manifestations (e.g., Barnett and Newell, 2008 and Ward et al., 2008). Therefore, in conjunction with mental imagery and creativity, increased positive and disorganised schizotypy may reflect a constellation of trait markers that are linked to synaesthesia. In this context, it is interesting to note that one mechanism that has been suggested to explain the relationship between increased schizotypy and both creativity and mental imagery is a difference in levels of inhibition/excitation (e.g., Grossberg, 2000 and Nelson and Rawlings, 2010).

Antibody activity against the C. d. collilineatus, C. d. cascavella and C. d. marajoensis venoms were found with all the antivenoms, although those venoms were not used in the immunization schedules (with the exception of C. d. collilineatus, which was

used in the Instituto Butantan’s immunization schedule). The antibody affinity for C. d. terrificus crude venom, crotoxin and PLA2 was evaluated by ELISA with the addition of KSCN in increasing concentrations as this website a chaotropic agent ( Fig. 5). The antivenoms provided by the Instituto Butantan showed the highest affinity for the antigens used. The affinity scores from the three Experimental Groups were lower, and there was no difference between them. The lethal dose 50% (LD50) of C. d. terrificus venoms was calculated to be 1.2 μg per animal. Neutralizing activity was assessed by injecting Swiss mice (18–20 g) with serial dilutions of antivenoms and 5 LD50 of venom, and neutralization

was calculated by probit analysis. Results are expressed as the volume of antivenom (mL) required to neutralize 1 mg of venom ( Fig. 6). Antivenom and plasma provided by the Instituto Butantan showed a great neutralizing capacity, with 2.18 mL and 2.42 mL check details required to neutralize 1 mg of venom, respectively. Plasma from Experimental Group 1 displayed a low neutralizing action, with 6.15 mL required to neutralize the venom. Plasma from Experimental Group 2 showed the highest neutralization capacity among the three Experimental Groups, although it was still lower than the commercial antivenoms, requiring 3.80 mL to neutralize 1 mg of venom. Plasma from Experimental Group 3 showed the lowest neutralizing capacity, with 6.68 mL needed to neutralize the venom. Using the in vivo neutralization selleck kinase inhibitor data and the protein concentration of the antivenoms, we were able to calculate the specific activity against C. d. terrificus venom ( Table 1). The production of anti-snake venom antibodies

to treat victims bitten by venomous snakes was originally developed in France at the Institute Pasteur (Calmette, 1894) and later developed and greatly expanded by Vital Brazil (Brazil, 1901, 1903). Crude venoms and horses were the immunogens and animals producing the antibodies, respectively. Once the antivenom effectiveness was demonstrated, the original procedure, although preserved in essence, evolved as dictated by progress in fields such as carbohydrate, lipid, and protein chemistry and basic immunology. For example, the serum protein cleavage by pepsin (Pope, 1936), with the clear objective of reducing the amount of heterologous protein injection into the victims. In addition to cleaving several non-antibody proteins, pepsin cleaves the Fc region of the IgG molecule generating a single, active, bivalent antigen-binding fragment, F(ab′)2 (Nisonoff et al., 1960).

The data obtained for macronutrients and energy value for different mousse trials were compared with the current Brazilian legislation (ANVISA, 2003a, ANVISA, 2003b, ANVISA, 2005 and Brasil, 1998) and their Olaparib mouse changes under updating (ANVISA, 2011), as well as the regulatory standards for nutrition labelling and claims in the European Union (E.U.) and the United States (U.S.) (EC, 2007, US CFR, 2010a, US CFR, 2010b, US CFR, 2010c, US CFR, 2010d, US CFR, 2010e and US CFR, 2010f). The control mousse MF was used as the standard formulation whenever a reference product was

required for comparisons. Statistical analysis was performed for total solids, fat, protein, DFotf, mineral elements, and FA composition data. Homogeneity of variance among samples was analyzed using Cochran and Bartlett tests (P < 0.05). Samples with homogenous variance were analyzed using one-way analysis of variance (ANOVA) followed by Tukey post-hoc test in order to identify contrasts

among samples (P < 0.05). The equivalent non-parametric tests were applied when a non-homogeneous variance selleck chemical was observed (P < 0.05). The chemical composition of mousses is shown in Table 3. Although solid content of mousses was very close, about 36 g/100 g, significant difference was observed (P < 0.05), which might be expected for this kind of product, due to some variations during manufacture (proportion of evaporated water during pasteurization, for e.g.). Mousses I and MF–WPC showed minimum and maximum solid content, respectively. Ash Selleck 5-Fluoracil content was less than 1 g/100 g for all mousses studied and even though there were only slight variations among samples, statistical differences were observed (P < 0.05). Control mousse (MF) and WPC showed minimum and maximum ash content, respectively.

Whey protein concentrate seems to have slightly contributed for increased ash content in mousses MF–WPC, I–WPC, and MF–I–WPC, in which fat was partially substituted by this ingredient. Major contribution to ash content may be attributed to the milk-derived ingredients in all mousse formulations. Within the mineral elements analyzed, Ca was found in higher levels, followed by Mg, in particular for mousses I and WPC. Lower content was found for Cu, followed by Zn and Fe. Significant differences observed between samples for mineral elements (P < 0.05) did not clearly evidence that such changes could be attributed to the different combination of ingredients used in mousse formulations. Nonetheless, these results were expected, considering a milk-based product, especially regarding the Ca, Mg, and Zn amounts. The Institute of Medicine (IOM) recommends 1000 mg Ca per day for adult males and females between 19 and 50 years old ( IOM, 2011). For Mg, the same institution recommends 420 mg and 320 mg per day, respectively, for adult males and females 31 years or older ( IOM, 2001).

Data are expressed using means±SD. Statistical analyses were performed using PASW statistics 18 software (IBM SPSS, NY, USA). The amplitudes and the latencies for source activities and the locations of ECD were statistically analyzed using one-way repeated measures ANOVA. The differences in the increased ratio of the source activities accompanying the increase in pin number or stimulus intensity were also analyzed using one-way repeated measures ANOVA in order to compare the responses from MS and

ES. The sphericity of the data was analyzed using Mauchly′s test, and Greenhouse–Geisser-corrected significance values were used when sphericity was lacking. Tukey′s HSD was used for multiple comparisons. For all analyses, differences were considered significant at the p<0.05 level. The present study was supported by a Grant-in-Aid for scientific research (B)22300192 from the Japan Society Sunitinib nmr for the Promotion of Science (JSPS) and a Grant-in-Aid program

from Niigata University of Health and Welfare (H24B05). “
“Cerebral ischemia-reperfusion causes injury to brain tissues, including neurons, glial cells, and cerebral blood vessels, resulting in their dysfunction. BIBW2992 in vitro Numerous studies have revealed the possible factors that cause cell damage and the therapeutic targets of cerebral ischemia-reperfusion injury. For instance, massive release of glutamate into the extracellular space, induction of oxidative stress, and generation of proinflammatory cytokines occur during or after ischemia. Suppression of these events attenuates ischemic insults (Lakhan et al., 2009, Mehta et al., 2007, Nakka et al., 2008, Park et al., 1988, Peters et al., 1998 and Tuttolomondo et al., 2009). There are two regions in an ischemic brain: the ischemic core and the penumbra. In the ischemic core region, neurons and glial cells suffer severe injury characterized by necrosis and their

function is irreversibly impaired during the acute phase selleck chemical of ischemia-reperfusion. In the penumbra region, cell insults are moderate and cell death due to apoptosis progresses for several days (Ueda and Fujita, 2004). Research into agent intervention to save cells from cell death in the penumbra region is ongoing (Barone, 2009 and Kaushal and Schlichter, 2008). We previously found a neuroprotective substance, serofendic acid, in a lipophilic extract of fetal calf serum. Serofendic acid is 15-hydroxy-17-methylsulfinylatisan-19-oic acid and a sulfur-containing atisan-type diterpenoid (Kume et al., 2002). It is a low-molecular-weight (mw 382) compound and exhibits potent protective effects on neurotoxicity induced by glutamate, NO, and oxidative stress without inhibiting glutamate receptors in cultured cortical, striatal, and spinal cord neurons (Kume et al., 2005, Kume et al., 2006, Osakada et al., 2004 and Taguchi et al., 2003).

33, right Z = 3.52 (all p < .001, uncorrected). On the TLT (Fig. 3) SRTs in controls demonstrated a bimodal distribution (Fig. 5A). One population peaked ∼280 msec after green onset, consistent with saccades made ‘reactively’ following the GO signal. In addition, there was an early population with a peaking 63 msec after green onset. To demarcate these two distributions we used linear rise-to-threshold modelling, assuming two independent processes,

the first triggered by amber light onset and the second by the green light (Adam et al., 2012). The early, anticipatory responses were further divided into errors (saccades before green onset) and correct anticipations (saccades after green onset, but planned in advance of it). ‘Reactive’ saccades were classified as those after 200 msec (see BIBW2992 cost Methods). Controls demonstrated a high proportion of early responses (mean 42% saccades, SD 18.95). Half

were correct anticipations (21%, SD 8.64). The rest were errors (21%, SD 14.35). Overall mean Correct Anticipations: Errors Ratio (CA|ER) ratio was 1.53 (SD .87), with mean reward 18p/trial (SD 4.6p). CA|ER correlated well Selleckchem JQ1 with mean reward obtained (R2 = .77; p < .0001). In contrast, KD's distribution of saccades was unimodal, with most made after green onset (Fig. 5B). Nearly all his eye movements were reactive, with only 8.0% early responses, significantly different from controls (Z = 2.8, p = .003). Furthermore, the majority of these were errors; correct anticipations formed only 2.2% of saccades (Z = 2.8, p = .003). His CA|ER was .4 and he obtained only 14p/trial. Within the first session, controls gradually increased the proportion of early responses (Fig. 6A), with a significant difference between the first PRKACG 100 trials (30.5% early responses, SD 25.20) and the third (44.6%, 21.24; p < .05). There was also a trend for CA|ER to increase from the beginning to the end of the session (p = .08). In contrast to controls, KD showed no evidence of learning

with 8% early responses in the first 100 trials to 7% in the last ( Fig. 6A). On the directional reward-sensitivity saccade task (Fig. 4) controls showed a small, but significant SRT advantage to the RS (mean RS 206 msec vs US 219 msec; p = .03) ( Fig. 7). This sensitivity to reward did not change significantly over the first session [analysis of three forty-trial epochs F(5,66) = .24, p > .9]. By contrast, KD showed no significant difference between rewarded versus unrewarded saccades (mean US = 236 msec vs RS = 235 msec; p > .5; Fig. 7), and there was no significant change across epochs. His SRTs were longer than control means but within normal range. On the TLT, KD’s performance altered dramatically 1 h after a single dose of l-dopa 100 mg (Figs. 5C and 6B). His early responses increased, with a CA|ER of 4.20 (6.67 SD > control mean of 2.20, SD .30) and overall increase in reward. Over the session, his early responses increased (14% in first 100 trials to 43% in the last; Fig. 6B).

Of 122 primary human resected PDAC, fascin was absent from normal ductal and acinar tissue, but prominent in PDAC cytoplasm (Figure 1A). Ninety-five percent of human PDAC expressed fascin and a high histoscore significantly correlated with decreased overall survival ( Figure 1B), see more high tumor grade ( Figure 1C; median histoscore 104.4 vs 72.8; P < .05), and vascular invasion ( Figure 1D; median histoscore 94.5 vs 62.2; P < .04). Fascin levels did not correlate with lymph node status, tumor stage,

perineural invasion, and lymphatic invasion (data not shown). In a multivariate Cox proportional-hazards regression analysis, high fascin expression only reached borderline significance as an independent predictor of poor survival, with a hazard ratio of 0.663 (95% confidence interval: 0.44−1; P = .05) ( Supplementary Table 1). Importantly, fascin levels strongly

correlated with time to recurrence, indicating potential importance as a predictor of tumor dissemination ( Figure 1E; P < .0005). To explore a functional role of fascin, we used a mouse model of pancreatic cancer (KPC mice) recapitulating both pre-invasive PanIN (grade 1−3) and invasive, metastatic PDAC.4 Wild-type ducts and acini and PanIN1−2 from 10-week-old KPC mice were negative for fascin (Figure 1F). Around 6% of PanIN3 and 100% of PDAC (both 10-week and advanced tumors) ( Supplementary

Table 2) were fascin positive ( Figure 1F) Galunisertib order and fascin was expressed in both well and poorly differentiated areas (data not shown). Fascin null mice had normal-sized pancreata with no apparent changes in tissue structure or proliferation (Supplementary Figure 1). Although fascin is weakly expressed Loperamide by a few cells in the islets of Langerhans (Figure 1F), fascin null mice had normal peripheral blood levels of several markers indicating normal pancreatic function ( Supplementary Table 3). Development of PanIN in KrasG12D or KrasG12D and p53R172H expressing pancreata was not changed by loss of fascin ( Supplementary Figure 2). Loss of fascin also did not affect progression, morphology, or proliferation of cells in an acute model of pancreatitis using cerulein injection ( Supplementary Figure 3). However, by 21 days of cerulein treatment, fascin was detected in stroma and epithelium of PanIN of KC animals ( Supplementary Figure 3). However, loss of fascin did not affect the numbers of monocytes, lymphocytes, or neutrophils recruited to acute PanINs, revealing no gross abnormalities in the immune response to PanIN in the fascin null mice ( Supplementary Figure 3E and F). In summary, fascin expression was detected in a minority of PanIN3 and all PDAC and loss of fascin did not detectably affect pancreas development or PanIN.

Very few phantoms for rodent cardiac MRI have been published. Li et al. [12] developed a static doughnut-shaped digital phantom for their work on myocardium imaging. Riegler et al. [13] described a phantom consisting of a heart extracted from

a rat within which was inserted a balloon that was inflated to learn more different volumes for calibration. Extending this to cyclic inflation would produce very realistic MRI data but with the disadvantage of requiring sacrifice of an animal, having a limited lifespan, involving biological tissues and not being easily reproducible by other labs. To date, there appears to be no reported work describing the design of a rodent phantom manufactured from readily available materials and not involving excised tissues or ex vivo preparations. The aim of this work was to close this gap by developing cardiac

phantoms suitable for rodent MRI. The phantoms were designed to provide realistic MRI data sets mimicking LV geometry and motion in the short-axis view. The main criterion was to mimic the dynamic behavior of the heart in the short-axis (“cross-sectional”) view of the left ventricle at midventricular level. The phantoms should produce plausible MRI images, be of the same general dimensions as mouse and rat left ventricles, and undergo similar distension and change in wall thickness. It was not the intention to model complex rotation and shortening movements

or to mimic ventricular blood flow patterns. Previous studies have used a number of materials to construct cardiac phantoms, see more including agarose [6], latex [14], silicone [7], [11] and [15] and PVA Cryogel [10]. The latter material is a gel, which has been used in the construction of ultrasound and MRI-compatible phantoms [16], [17], [18] and [19]. Edoxaban The gel is converted into an elastic solid by undergoing a number of freeze–thaw cycles. The elastic modulus and relaxation times T1 and T2 are controlled by the number of cycles, typically ranging between 2 and 10. PVA Cryogel was chosen for construction of the cardiac phantoms in this study because of the ability to readily control the characteristics of the material. For cyclic distension of the phantom, two approaches were considered, namely, local activation and remote activation. Remote activation has been used in previous studies involving connection of the chamber to a remote pump via stiff tubing [9] and [11]. The potential disadvantage of this technique is loss of pulsatility due to some unavoidable elasticity of the tubing. Local activation could involve generation of a force close to the phantom. Possibilities might include use of the scanner’s B0 magnetic field itself [20]. Though local activation would have been a technically elegant solution, a remote method was chosen as it is simple to implement and has worked in previous published studies.

Artificial light disturbs this activity. Community changes arising Trichostatin A in vitro from light pollution may have knock on effects for ecosystem functions ( Gliwicz, 1986 and Gliwicz, 1999). Even remote areas can still be exposed to sky glow. Along the expanding front of suburbanization,

light may spill into wetlands and estuaries that are often the last open spaces in, or close to, cities ( Longcore and Rich, 2004). Perhaps surprisingly, light pollution penetrates into deep ocean environments (Kochevar, 1998). Here, only very dim, homochromatic, down light is available, supplemented by bioluminescence from marine organisms. Most inhabitants possess highly specialized visual systems, which are incredibly sensitive to even minute amounts of light. This renders these organisms extremely vulnerable to damage associated with bright artificial lights of manned and unmanned submersible vehicles (Kochevar, 1998). The current efforts to deal with the oil well disaster in the Gulf of Mexico find more has revealed the extent to which light pollution can occur in the deep sea, albeit that the effects are secondary to the effects of oil pollution in this case. There is a widely held, but incorrect belief that organisms living in caves (whether under the sea or under

land masses) do not come into contact with light and are therefore insensitive to it. However, as with deep sea creatures, many cave dwelling organisms are bioluminescent and are exquisitely sensitive to any ambient light and light pollution. Most if not all, cave dwelling organisms and others living remotely from daylight, evolved from organisms that at one time dwelt in the light and hence retain vestiges of light sensing systems. Over the last ca. 150 years there has been an exponential increase in the use of artificial light to illuminate the night. This trend continues to this day. On land, street lights, lighting in office buildings and homes, and floodlit sports facilities, industrial complexes, etc., are the sources which inadvertently introduce light into nature (RCEP,

2009). In coastal areas, where many of our major cities such as Mumbai, Shanghai, Alexandria, Miami, New York City and London are located, long stretches of the shoreline are strongly illuminated. Indeed, light pollution of shallow seas has become a global phenomenon (Elvidge et al., Interleukin-3 receptor 1997). There are at least 3351 cities in the coastal zones around the world shedding light onto beaches and into sublittoral areas. In Asia, 18 of the region’s 20 largest cities are located on the coast, on river banks or in deltas. Even in Africa where the availability of electric lighting is sometimes limited, coastal light pollution is emitted from major cities such as Abidjan, Accra, Algiers, Cape Town, Casablanca, Dakar, Dar es Salaam, Djibouti, Durban, Freetown, Lagos, Luanda, Maputo, Mombasa, Port Louis and Tunis (UN-HABITAT, 2009).