08) due to the low number of samples and the weak expression of TRP-2 in the metastases ( Figure 1B). In addition, we found also a significant decrease of TRP-2 positive cells in cell culture compared to their matched primary tumor tissue (p = 0.01; Figure 1C).

These findings indicate the survival benefit of TRP-2 negative cells in cell culture. Using our newly developed co-staining of Mib-1 and TRP2, we analyzed the proliferating (MIB-1 positive) melanoma cells depending on their TRP-2 expression in primary melanoma, and metastases (Figure 2A-D). In melanoma metastases, proliferating TRP-2 negative cells were significantly more frequent compared to the primaries (p = 0.01; Figure 1D), whereas non-proliferating TRP-2 positive cells were significantly less frequent in melanoma metastases compared to the primaries (p = 0.01). For the subgroups, which were http://www.selleckchem.com/products/GDC-0980-RG7422.html either negative or positive for both markers, we found no significant difference Selleckchem Afatinib between primary melanomas and metastases. Interestingly the percentage of TRP-2−/Mib-1+ cells significantly correlated with Breslow tumor thickness in the patient group with Breslow tumor thickness over 1 mm (p = 0.048; Spearman’s correlation coefficient 0,3). Furthermore, these cells were significantly correlated with Hif-1α expression (p = 0.03; Spearman’s correlation coefficient 0,3) and therefore with hypoxic condition in primary melanoma. In addition patients

who had less than 15% of TRP-2−/Mib-1+ in their primary melanoma had statistically an approaching significance for a better tumor specific survival (p = 0.05; Figure 1E). Melanoma patients’ cell cultures expressed significantly less Melan A than primary melanomas (p = 0.001) or metastases (p = 0.001; Figure 1 F). In addition TRP-2 was significantly less expressed in cell cultures if compared to primaries (p = 0.001) or to metastases (p = 0.02; Figure 1A). Hif-1α expression was significantly

higher in melanoma metastases (p = 0.04) and cell cultures (p = 0.0001) when compared to Montelukast Sodium primary melanomas (Figure 1G). Analysing all melanoma samples primary melanomas, metastases and melanoma cell cultures we found a significant correlation between Hif-1α expression and the the presence of TRP-2−/Mib-1+ cells (p = 0.002; Spearman’s correlation coefficient 0,2) as well as with proliferation (Mib-1) alone (p = 0.01 Spearman’s correlation coefficient 0,2). However, analysing separately the different groups, only a significant correlation between Hif-1α expression and the presence of TRP-2−/Mib-1+ cells in melanoma patient’s cell cultures persisted (p = 0.01; Spearman’s correlation coefficient 0,3). We found no significant correlation between Hif-1α, and TRP-2 expression neither in primary melanoma, melanoma metastases nor melanoma cell cultures as expected by cell line experiments. We treated primary human melanoma cell cultures with hypoxia for 72 hours and subsequently performed qRT-PCR for TRP-2 (Figure 3C).

g. biotin) uniquely enables global quantitative analysis of protein lipidation by enrichment coupled to standard liquid chromatography-mass spectrometry. In this review we discuss the development RO4929097 mouse of chemical

proteomics technologies that have resulted in the first quantitative whole-proteome studies of the known major classes of protein lipidation, and the first insights into their full scope in vivo. The most-well characterized form of protein N-acylation is N-terminal N-myristoylation, the irreversible attachment of a C14-fatty acid (myristate) to the N-terminal glycine of substrate proteins, which is catalyzed by N-myristoyltransferase (NMT) [ 4]. NMT is encoded by a single copy gene in lower eukaryotes, whereas in humans and Stem Cells inhibitor most other higher organisms two NMT genes (nmt1 and nmt2) have been identified. Protein N-myristoylation increases affinity for membranes and is required for viability and survival in every organism in which its essentiality has been studied. Dysregulation of myristoylated proteins has been linked to several diseases and NMT has been proposed as a potential drug target in viral, fungal, bacterial or parasitic infections, as well as in cancer [ 4]. Chemical tools have been developed to study N-myristoylation, including alkyne and azido-tagged analogues of the natural lipid

substrate (YnMyr and AzMyr, respectively) [ 5], as well as competitive inhibitors of the protein binding Bupivacaine site of NMT. YnMyr is used in most recent studies as it is known to give minimal background labeling [ 6], and alkyne-tagged lipids appear to recapitulate endogenous lipid metabolism [ 7]. Potent NMT inhibitors have also been reported, for example against NMT from yeast [ 8] and from Trypanosoma brucei (the causative agent of human sleeping sickness) [ 9 and 10], although these had variable selectivity against NMT from various species. More selective inhibitors

have been reported recently [ 11], and can be used as selective chemical tools to pharmacologically knockdown N-myristoylation in different organisms. However, metabolism (e.g. chain elongation) of N-myristoylation probes can result in trafficking into unrelated lipidation pathways including GPI anchors and S-palmitoylation (see following sections). In this context, the combination of NMT inhibitors with YnMyr and quantitative proteomic analysis has proven particularly powerful in establishing the N-myristoylated proteome in vivo, without interference by off-target protein labeling. In this approach, the response of YnMyr-tagged proteins to selective NMT inhibitors is quantified, and correlated with the identification of each protein as a substrate or non-substrate of NMT.

2001). As expected from previous studies (Suursaar et al., 1995, Astok et al., 1999 and Raudsepp et al., 2011),

our results of cumulative fluxes also indicated an annual net outflow in the Suur Strait. The northward fluxes (on average approximately 60 km3 yr− 1) were somewhat larger than those calculated by Raudsepp et al. (2011) for 2008 (23 km3 yr− 1). The difference could have occurred for several reasons. Firstly, Raudsepp et al. (2011) admitted that their (single-point) measuring site, which was at the depth of 3.5 m on one side of the strait, might not fully represent the Alpelisib mouse whole cross section. Also, the wind stress from the HIRLAM (High Resolution Limited Area Model) could have underestimated the winds above the narrow strait, as the corresponding model cells probably included land surface properties. On the other hand, as indicated by the long-term average wind speed at Kihnu (5.66 m s− 1 in 1966–2011 vs.

4.15 m s− 1 at Virtsu), our forcing may have overestimated the winds above the Väinameri part of the model domain. Finally, unlike Raudsepp et al. (2011), our calculations included constant 32 km3 yr− 1 inflows from rivers into the Gulf of Riga. (The seasonal variations in discharges have been largely controlled by the Riga Hydroelectric Power Plant on the River CP-868596 solubility dmso Daugava since 1974.) Although the larger part of that discharge ought to ‘flow out’ through the Irbe Strait, no one has any certain knowledge Ribonucleotide reductase of the actual proportion. In general, the inflow through the Irbe Strait should mirror the outflow through the Suur Strait, but in the relatively wide Irbe Strait under certain conditions in- and outflow can take place simultaneously (Lilover et al. 1998). The question could probably be solved either by studying Lagrangian

particle tracks (like Zhurbas et al. (2010) did in the Baltic Proper), or water ‘age’ (see e.g. Andrejev et al. 2004). Summarizing the problem for the Gulf of Riga, the interannual proportions as well as climatological shifts should remain the same, even though the exact magnitude of flows is unknown. Being differently exposed (Kõiguste to SE, Matsi mostly to S-SW), the locations showed a rather different wave time series (Figure 10). According to formal linear trends, the average wave heights have probably decreased at both locations. While at the windward Matsi the overall linear trend decreased very slightly in 1966– 2011, the trend was a significantly falling one near Kõiguste (Figure 10a). However, on the basis of annual maxima and higher quantiles (90%, 99%), the trends increased near Matsi, but still decreased near Kõiguste (Figure 10c,d). Especially at Matsi, the wave heights showed some quasi-periodic cycles with high stages in 1980–1995 and again after about 2007. The cycles basically followed those in atmospheric processes (Figure 9; Jaagus et al. 2008).

Unless infection occurs, a slight inflammation at the puncture site can arise. Spiders of the family Theraphosidae have AZD6244 order urticating hairs covering their bodies, which are brushed off by the spider as a mechanism of defense to deter predators. These hairs were found to induce local dermatitis in vertebrates, including humans ( Shrum et al., 1999). The puncture wounds from the spider’s fangs require local wound care, follow-up

for signs of infection, short-term analgesia and a tetanus booster ( Kelley and Wasserman, 1998; Shrum et al., 1999). The spider venom is a diverse mixture of low molecular mass compounds (16% of all compounds), acylpolyamines (11%), linear peptides (6%), cysteine-knotted mini-proteins (60%), neurotoxic CT99021 supplier proteins (1%) and enzymes (6%) (Jackson and Parks, 1989; Kuhn-Nentwig et al., 2011). It is mainly used to paralyze prey and for defense, and contains toxins that affect the central or peripheral nervous systems. These neurotoxins have been identified mostly as acylpolyamines and peptides or proteins that act on membrane receptors or ion channels (see review Estrada et al., 2007). The acylpolyamine toxins

are low molecular mass compounds (<1 kDa) that appear to have evolved to specifically provoke rapid paralysis. Their complex structures are composed by a polyamine chain with a primary amino or a guanidine group at one end and an aromatic ring at the other. These compounds interact with multiple targets in the central and peripheral nervous systems of insects, and also in the CNS of mammals, whereas the main targets are ionotropic

glutamate and nicotinic acetylcholine receptors (Kawai et al., 1982; Herold and Yaksh, 1992; Bixel et al., 2001). Eight hundred curated sequences of protein toxins have been described for spider venom to date, among them approximately 20% corresponds to Theraphosidae spiders (available at ArachnoServer 2.0; Herzig et al., 2011). Most of these 200 peptides has 30–40 amino Tacrolimus (FK506) acid residues, three disulfide bridges and basic character (Escoubas and Rash, 2004), and are modulators of ion-channels, such as calcium, sodium, and potassium. In this communication we report the results of proteomic and pharmacological characterizations of the venom extracted from the Brazilian spider Acanthoscurria paulensis. A. paulensis (Theraphosidae, Mygalomorphae) is a dark brown colored spider widely distributed in three Brazilian regions: South, Southeast and Midwest ( Mello-Leitão, 1923; Lucas et al., 2010).

This raises important questions about the lack of a significant correlation between WT1 expression levels and survival, despite the observation that WT1 acts as an oncogene and is highly expressed in more aggressive histological subtypes. WT1 is spliced alternatively at two sites: exon 5 with

17AA and the KTS site, which exists between exons 9 and 10. Splicing at these sites yields four variants (− 17AA/− KTS, + 17AA/− KTS, − 17AA/+ KTS, and + 17AA/+ KTS) [20], [21], [22] and [23]. Several studies have reported that the four WT1 splice variants have different functions in various cancers. NVP-BKM120 cell line WT1 + 17AA/− KTS induces programmed cell death through transcriptional repression of the EGFR gene in osteosarcoma cells [24]. WT1 + 17AA/+ KTS can cause a morphological transition from an epithelial phenotype to a more mesenchymal phenotype in mammary epithelial cells [25]. In ovarian cancers, WT1 − 17AA/− KTS induces morphological changes and promotes cell migration and invasion in vitro [20]. Moreover, Anticancer Compound Library purchase a recent study investigated the expression of WT1 splice variants using real-time PCR and reported that the ratio of WT1 variants, particularly + 17AA variants, is probably crucial for the process of malignant transformation in acute myeloid

leukemia [26]. Therefore, it is possible that the ratio of expressed WT1 splice variants is associated with the lack of a significant correlation between total WT1 expression and survival in patients with

ovarian cancers. Therefore, in this study, we examined four WT1 splice variants having distinct functions in ovarian tumorigenicity using stable ovarian cancer cell lines overexpressing each splice variants. We also examined the effects of WT1 variants on tumor growth, dissemination, and ascites production using an ovarian cancer mouse model. The RG7420 datasheet SKOV3ip1 cell line was generated from ascites developed in nu/nu mice by administering an intraperitoneal injection of human ovarian carcinoma cell line SKOV3 [27]. The SKOV3ip1 cell line was cultured at 37°C in M199:105 medium with 10% fetal bovine serum (FBS) and 1% penicillin-streptomycin in a humidified atmosphere of 95% air and 5% CO2. Four pcDNA 3.1(+) vectors (Invitrogen, Carlsbad, CA, USA) were engineered to contain one of the four human WT1 splice variants (− 17AA/− KTS, + 17AA/− KTS, − 17AA/+ KTS, or + 17AA/+ KTS) [20]. The sequences of each of these four WT1 variants were amplified from the corresponding vector by PCR using primers containing BglII and NotI restriction sites (sense primer sequence, 5′-AGA TCT GAC TTC CTC TTG CTG CA-3′; antisense primer sequence, 5′-GCG GCC GCT TGA AAG CAG TTC ACA CAC T-3′), digested, and ligated into the lentiviral vector plasmid, pHR-SIN-CSGW dlNotI [28] (a gift from Y. Ikeda, Mayo Clinic, Rochester, MN, USA).

A decrease in heart rate was observed in animals treated with atenolol alone (286 ± 1 beats/min vs 301 ± 1 beats/min, before; n = 5) or associated to Ang-(1–7) (278 ± 1 beats/min vs 293 ± 1 beats/min, before; n = 5). As shown in Fig. 1B, on the eighth week of treatment there was no change in fasted glycemia in any of the

groups. Although atenolol alone had a trend to increase glucose levels, values were not statistically selleck inhibitor different. In order to evaluate lipid profile, at the end of the 14 weeks of treatment, total serum cholesterol, glycerol and triglycerides were measured. As shown in Fig. 1C, CD-Ang-(1–7) or atenolol alone did not alter serum triglycerides. However, animals

that received the association of CD-Ang-(1–7) and atenolol presented a ~60% lower values of total serum cholesterol (13 ± 3 mg/dL; Fig. 1D) than control animals that received CD alone, vehicle (38 ± 5 mg/dL; Fig. 1D). After oral administration of fat load, a hypertriglyceridemia was observed in control (vehicle; 92 ± 33 mg/dL vs 34 ± 3 mg/dL, before; find more Fig. 2A) or animals treated with atenolol, with a peak at 210 min (115 ± 17 mg/dL vs 52 ± 6 mg/dL, before; Fig. 2A). This alteration was not observed in the other groups: CD-Ang-(1–7) alone (52 ± 10 mg/dL vs 35 ± 6 mg/dL, before; Fig. 2A) or in CD-Ang-(1–7) associated with atenolol (48 ± 8 mg/dL 38 ± 4 mg/dL, before; Fig. 2A). Lipolysis was measured by the release of glycerol at baseline and after isoproterenol stimulation or insulin inhibition. As expected, isoproterenol

increased glycerol release in all groups (Fig. 2B). Although the basal lipolysis was similar in all treatments, after isoproterenol stimulation, the association of CD-Ang-(1–7) and atenolol induced a greater lipolysis (120 ± 14 mg/dL; Fig. 2B) as compared to atenolol alone (82 ± 7 mg/dL; Fig. 2B). Interestingly, the sensitivity of insulin was not changed by any treatment (Fig. 2C). Further, the sensitivity of insulin on glucose uptake was measured Ponatinib order in adipocytes by radioactivity into the cells, since 2DOG can be transported but not oxidized. We have observed that all treatments did not change glucose uptake or the insulin sensitivity (Fig. 2C). Lipoprotein lipase (LPL) is an enzyme that hydrolyzes triglycerides components of lipoproteins providing free fatty acids (FFAs) and monoacylglycerol for being used by tissues. The release 3H-FFAs was quantified by liquid scintillation as an estimative of LPL activity. As shown in Fig. 2D, the LPL activity was not different in all groups studied. The present study showed, for the first time, the metabolic effect of an oral treatment with Ang-(1–7) associated with the β-blocker-atenolol.

, 2005). MGO also increased the generation of hydrogen peroxide in VSMCs and increased formation of peroxynitrite (ONOO–) through the induction of inducible NOS (iNOS) (Chang et

al., 2005). Similar results were found by Ward buy Carfilzomib and McLeish, who added MGO in neutrophils and found that there was a significant increase in basal production of hydrogen peroxide and superoxide anion in a dose-dependent manner of the MGO concentration, indicating increased respiratory burst activity (Ward and McLeish, 2004). The effect of MGO was significantly higher in platelets pretreated with an agent that depletes GSH and glutathione peroxidase (Leoncini and Poggi, 1996). Contrasting with these results, our data show that MGO/high glucose did not cause any major change in the production of reactive oxygen/nitrogen species in neutrophils (Fig. 3). One acceptable reason for the weak pro-oxidant effect of MGO/high glucose could be the MGO concentration used in the present study. Many authors demonstrate a modulation of MGO on different cell types using high MGO concentrations ranging from 100 μM to 1 mM (Chang et al., 2005, Desai et al., 2010 and Wang et al., 2009). We used MGO at 30 μM, which is considered by some authors a high concentration usually found in the diabetic plasma (Dutra et al., 2005). In http://www.selleckchem.com/products/BAY-73-4506.html addition,

the incubation time of neutrophils which MGO/high glucose could be short to promote any permanent modification in the neutrophil function. Several authors have shown that, to be effective as a glycation agent, MGO needs to be incubated for long periods, which was not observed in this work, Ketotifen due to the short half-life of neutrophils in culture. On the other hand, association of astaxanthin with vitamin C promoted a clear antioxidant effect (Fig. 3) as observed by the marked reduction in the production of superoxide anion and hydrogen

peroxide production. Compared with a previous study from our group that showed a weak astaxanthin antioxidant-effect (Bolin et al., 2010, Campoio et al., 2011, Guerra and Otton, 2011 and Macedo et al., 2010), the association of both antioxidants allowed a great antioxidant action. Many authors have reported the effective antioxidant action of either astaxanthin or vitamin C alone, but not in combination. In our model, the astaxanthin/vitamin C system mimics the recycling system of vitamin C/vitamin E. Astaxanthin provides cell membranes with potent protection against free radicals or other oxidative attack. Experimental studies confirm that this nutrient has a large capacity to neutralize free radicals or other oxidant activity in the nonpolar (“hydrophobic”) zones of phospholipid aggregates, as well as along their polar (hydrophilic) boundary zones (Fassett and Coombes, 2011). Vitamin C, in turn, promotes antioxidant effects mainly in water-phase microenvironment.

Remineralization at the bottom is assumed to be proportional to the amount of available benthic detritus, at a constant rate rD. The set of constants is given in Appendix A. There now follow a few remarks regarding their choice. For the grazing formulation, the threshold value Phyto and the half-saturation value kPhyt have been changed according

to data reported by Dzierzbicka-Głowacka (2005). The nitrogen to carbon ratio gN is assumed to be 0.013 mmolN (mgC)−1, the half-saturation constant for total inorganic nitrogen is 0.5 mmolN m−3, and the optimal light intensity for the phytoplankton community is set at 60 W m−2. For the remineralization rates in the water and at the KU-60019 molecular weight bottom (following Postma & Rommets (1984)) ca 20% of the average labile particulate organic carbon (POC) is mineralized daily. Thus, 20% of the POC formed as detritus is remineralized instantaneously (pF = pM = pZ = 0.2), whereas the remaining 80% is transported immediately to the bottom. There is no

explicit sinking of living phytoplankton, because this is already included in the instantaneous transfer to the bottom ( Figure 2). Ingested material is divided equally between dead zooplankton, faecal pellets and soluble excretion following Steele (1974). The benthic nutrient mineralization rD is taken to be 0.0005 day−1 exp(0.005°C−1T) ( Savchuk & Wulff 1996). The intention was to simulate selleck screening library production in a physical environment that would be as realistic as possible. Actual oceanic forces are required for reliable simulations of phytoplankton dynamics (Figure 2). The external forcing is taken from ECMWF (ERA 40 reanalysis, www.ecmwf.int). The biological reaction terms are

not implemented in the circulation model. The primary production model is an independent transport model that uses the circulation model output, so there is no feedback from Evodiamine the biology to the physics, which makes the simulations easier to implement. Another important force for primary production simulations is solar radiation with its own daily cycle. The total irradiance at the surface is calculated using the model by Rozwadowska & Isemer (1999). The local weather conditions were recorded on board Voluntary Observing Ships, and these data have been used to estimate the climatological characteristics of the solar radiation flux at the sea surface. The monthly loads were interpolated to give daily values. Nutrient contributions from rivers are not included in this model, but the initial values for nutrients have been based on the SCOBI 3D-model. Phytoplankton production is limited in the model by light and total inorganic nitrogen. The phytoplankton biomass is restricted by mesozooplankton grazing. The zooplankton biomass is prescribed as a force and the model uses the abundance data from Mańkowski (1978), Ciszewski (1983) and Mudrak (2004) for the southern Baltic Sea.

Scores ≥11 are considered VE 821 to indicate probable clinical anxiety and depression (“cases”). Self-management ability was measured using the heiQ [25]. Patients are asked to rate items on a 4 point likert scale ranging

from “strongly disagree” (1) to “strongly agree” (4). Higher scores represent higher levels of self-management abilities. The eight scales are: positive and active engagement in life; health directed behavior; skill and acquisition technique; constructive attitudes and approaches; self-monitoring and insight; health services navigation; social integration and support; emotional well-being. Condition specific measures for COPD, depression, diabetes and pain were also collected at baseline and 6 months follow-up. Interviews were also conducted with patients and tutors across all 4 conditions. These data are reported separately in other publications [26]. All data analyses were conducted using IBM SPSS Statistics 20. The main analysis involved only those patients who attended ≥5 SMP sessions (defined as course completers) and returned 6 month follow-up questionnaires. The level of statistical significance Z-VAD-FMK nmr was set at p = 0.05. An intention to treat (ITT) analysis was also performed on all patients, irrespective of the number of sessions attended to ensure that the effectiveness of the program has not been overestimated. Missing 6 month follow-up data (T2) were replaced

with baseline (-)-p-Bromotetramisole Oxalate data, last observation carried forward.

Changes in the mean values of the patient outcomes were compared over time using paired t tests and General Linear Model for repeated measures. The outcome variables were normally distributed. For the main analysis only important prognostic factors such as age, gender, long-term condition, co-morbidity, number of sessions attended and socioeconomic factors (education, employment status) were adjusted for using analysis of covariance. Effect sizes (Cohen’s d) [27] were calculated using the following calculation: the mean score at 6 months minus the mean score at baseline divided by the standard deviation at baseline. Recommended boundaries [27] were used to determine small (0.2), moderate (0.5) and large effect sizes (0.8). The heiQ scale developers recommend a distribution-based cut-off of ES = 0.5 as a standardised cut-off [28]. Based on this cut-off, three categories of change were defined: ‘substantial improvement’ (ES ≥0.5), ‘minimal/no change’ (−0.50 < ES < 0.50), ‘substantial decline’ (ES ≤−0.5). We also looked the proportion of patients whose PAM scores improved by 4 points. Changes in “caseness” for anxiety and depression between baseline and 6 months follow-up were tested using McNemar’s test. In total, 1850 patients contacted the EPPCiC recruitment helpline, and of these, 563 (30%) patients did not register to attend the SMP.

Moreover, the strategy did not account for the high vulnerability and low resilience inherent in

fisheries resources in general. Prior to unification in 1990, the two separate entities of Yemen pursued different fisheries development policies; while the state in the north adopted a policy of supporting artisanal sector development, the state in the south pursued a policy of supporting large-scale industrial fishing [37]. After unification, the authorities encouraged a policy of supporting the artisanal sector development and gradually eliminated the agreements with the industrial fleets. As a result, the number of fishermen and fishing boats has increased rapidly and production estimates reached a peak of 256,300 t in 2004 before dropping to 130,591 t in 2008 [28]. The catch per unit of effort (CPUE) has simultaneously decreased with time [28], [38] and [39]. In Lenvatinib mw the absence of proper governance, industrial fleets have caused not only fish stock depletion but also major destruction to fish habitats [40] and [41]. In line with the announced fisheries

strategy that gives preference to the artisanal sector, new licenses for industrial vessels have not been granted since 2004. Currently, there is no licensed industrial fishing in Yemen and there are only a few coastal fishing fleets with illegal www.selleckchem.com/products/pf-562271.html licenses in the Gulf of Aden and the Arabian Sea, some of which operate with artisanal licenses. Industrial fleets are registered to fish for almost all different kinds of fish, including pelagic fish. However, reporting of catches have never included any pelagic fish. Moreover, it is believed that these trawlers are poaching significant quantities of tuna and tuna-like species. Furthermore, significant quantities of fish are being captured illegally by unlicensed industrial fleets; these fish are being transferred directly to other countries [32] and [42]. Due to the limited employment opportunities available to the coastal inhabitants, increased domestic demand, and the open-access nature of fisheries, the number

of fishermen Fenbendazole has increased rapidly. Moreover, the return of one million expatriates from Saudi Arabia after the 1991 gulf crisis [43] has also added to the numbers of workers entering artisanal fishing [40] and [41]. Subsequently, fishermen numbers have increased three-fold between 1990 and 2010 [28]. Most of the recent growth has occurred in the Red Sea region where both fishermen and fishing boats numbers have increased four-fold between 2000 and 2010 [28]. This rapid growth in the past decade is attributed, in part, to changes in national policy that have led to a reduction of the industrial fleet. Fish exports have witnessed significant increases and reached 110,000 t in 2010, which is nearly 58% of the total fish production [28].