The Pacific Krill (Euphasea Pacifica), for instance, was observed to ingest its staple algae

as well as polyethylene beads ground to about the same size range with no evident foraging bias ( Andrady, 2009). However, no studies have been conducted with plastic beads loaded with POPS; also, it is not known if any chemotactic or other warning signals that discourage their ingestion (as opposed to that of ‘clean’ plastic beads) by at least some of the species at risk, operate in nature. Table 2 Is a selection of some of the marine species shown to be able to ingest plastic beads in laboratory studies. Information on the bioavailability of sorbed POPS to the organism subsequent to ingestion of tainted microplastics by different species is particularly sparse. In marine NVP-BGJ398 lug worms, a deposit feeder, Voparil et al. (2004) demonstrated the bioavailability of PAHs in anthropogenic Nutlin-3a molecular weight particles such as tire tread, diesel soot placed in gut fluid. Gut surfactants in benthic deposit feeders possibly enhances the bioavailability of

POPs in these species (Voparil and Mayer, 2000 and Teuten et al., 2007). Especially with plankton species with a very small body mass, the quantity of POPs delivered via saturated microparticles could have a significant toxicological impact. The dose delivered will depend not only on the volume of microparticle ingested but also on its residence time in the organism and the kinetics of repartition

of the POPs between the plastic and tissue medium of zooplanktons. In larger marine species such as the Great Shearwater (Puffinus gravis) the amounts of ingested contaminated plastics and polychlorinated biphenyls (PCBs), DDE, DDT, and dieldrin) in adult fat tissue were positively correlated ( Ryan et al., 1988). No data is available on the transfer coefficients across marine trophic levels for POPS introduced via ingested microplastics. Engineered plastic nanoparticles derived from post-consumer waste as well as from meso-/microplastics via degradation triclocarban pose a specific challenge to the ecosystem. Though as yet not quantified, there is little doubt that nanoscale particles are produced during weathering of plastics debris. If these are able to persist as free nanoparticles once introduced into water medium is an important consideration. Nanoparticles in air and water readily agglomerate into larger clusters or lose aggregates with other material. Nanoparticles incorporated in these can still be ingested by filter feeders (Ward and Kach, 2009) but if they will have the same physiological impact of the primary nanoparticles is not known. Small Eukaryotic protists, Diatoms and Flagellates that measure in the range of 200 nm to a couple of microns are abundant in the oceans.

Overall, patients with positive margins (16.5 vs. 10.0 mm, p = 0.04) and the pooled close/positive-margin (11.0 vs. 10.0 mm, p = 0.03) patients had larger median tumor sizes than the negative-margin cohort. Also, patients with close (13.6 vs. 9.2%, p = 0.01) or positive (15.4% vs. 9.2%, p = 0.03) margins were more likely to be estrogen receptor (ER)

negative than the margin-negative CP-868596 chemical structure cohort. Positive-margin patients were more likely to be node positive as well (15.4% vs. 2.5%, p = 0.01). With regards to the invasive-only patients, those with positive margins were more likely to be node positive (18.2% vs. 3.4%, p = 0.02) than margin-negative patients. No differences in patient characteristics by margin

status were noted IDH assay when evaluating patients with pure DCIS, albeit with smaller numbers of patients. Of note, no differences in the rates of systemic therapy usage were noted for all patients. Clinical outcomes by margin status and disease histology are presented in Table 4. Overall, no statistically significant difference in the 6-year rate of IBTR was noted for patients with close margins compared with that of negative-margin patients (8.7% vs. 4.1%, p = 0.10) despite a nearly twofold increase. Positive-margin patients had a nonsignificant increase in IBTR (14.3% vs. 4.1%, p = 0.41); however, when both groups were pooled, a trend toward higher rates of IBTR in patients with involved margins was noted (9.3% vs. 4.1%, p = 0.07). Statistically significant increases in EFs were noted for close (6.8% vs. 2.6%, p = 0.04) and close/positive-margin (7.7% vs. 2.6%, p = 0.02) patients compared with negative-margin patients; however, no differences in TR/MM were noted. No differences emerged

in the rates of regional nodal failure, distant metastases, disease-free survival (DFS), cause-specific survival, or overall survival by margin status in the entire cohort. When examining invasive-only patients, no significant differences in the rates of IBTR were noted for patients with positive margins (20.0% vs. 4.1%, p = 0.30), those with close margins Thymidylate synthase (6.2% vs. 4.1%, p = 0.62), or those with pooled close/positive margins (7.5% vs. 4.1%, p = 0.43). Furthermore, no differences emerged in the rates of regional nodal failure, distant metastases, DFS, cause-specific survival, or overall survival by margin status for invasive-only patients. When evaluating patients with DCIS only, there was a statistically significant increase in IBTR when patients had close margins (17.6% vs. 4.2%, p = 0.004) and when close and positive margins were pooled (15.7% vs. 4.2%, p = 0.01). This significant increase in IBTR led to a nonsignificant reduction in DFS in patients with noninvasive disease who had close surgical margins (82.4% vs. 90.8%, p = 0.17). Statistically significant increases in EFs were noted for close-margin (17.6% vs. 1.5%, p < 0.

They also play the largest positive role in increasing loaf volume, while showing the lowest weakening effects on dough strength [4] and [5]. Functional analysis in vitro [10] of such contributions to wheat flours by the α-gliadin protein subunit ACX71610 (encoded by GQ891685 and carrying an extra cysteine residue in the C-terminal unique domain II) has been confirmed. But recent advances in the study of the pathogenesis of celiac disease (CD), a T-cell-mediated

chronic inflammatory disease with an incidence as high as 1% in many populations and caused by a permanent intolerance of dietary gluten, have also revealed that the α-gliadins are the major initiators of CD [11], [12], [13] and [14]. Based on the available literature, a variety of gluten peptides with proven in vivo SP600125 supplier or in vitro activity have been identified in gliadins as well as glutenins; however, their relative importance differs [15]. Only five peptides, one (glia-γ1: QQPQQSFPQQQ) occurring in γ-gliadins and four (glia-α9: PFPQPQLPY, glia-α2: PQPQLPYPQPQLPY, glia-α20:

PFRPQQPYPQ, and glia-α: QGSFQPSQQ) in α-gliadins, are dominant, and are generally referred to as the immunodominant peptides. They have been shown to be recognized BMN 673 in vivo by T-cells from almost all CD patients, both children and adults, whereas T-cell responses to other gluten proteins are much less frequent and generally appear in young CD patients. Furthermore, they elicit a stronger T-cell response and their immune activity

is designated as +++ compared to the + of the other epitopes [16], [17], [18], [19], [20] and [21]. Comparative analysis [13] of the deduced amino acid sequences of the full-ORF α-gliadin genes derived from several diploid wheat species representing the ancestral A (Triticum monococcum), D (Aegilops tauschii) and potentially ancestral B (Aegilops speltoides) genome of hexaploid bread wheat indicates CYTH4 significant differences in the average lengths of the two glutamine repeats, as well as the occurrence of the four major T-cell peptides in α-gliadins, according to their genomic origin. The α-gliadins derived from the A genome almost invariably contain only glia-α9 and glia-α20 and carry a larger average number (27.7 ± 1.7) of glutamine residues in the glutamine repeat I than do the B (20.0 ± 3.4) and D (20.7 ± 1.1) genomes. The α-gliadins originating in the B genome usually lack such immunogenic peptides or contain only glia-α and carry a larger average number (18.8 ± 1.9) of glutamine residues in the second glutamine repeat than do the A (10.2 ± 0.6) and D (9.7 ± 1.4) genomes.

001). We also examined the time course of hippocampal expression of the NFκB and IRF3-dependent

gene interferon-inducible protein 10 (IP-10). This chemokine mRNA showed a very similar temporal pattern of induction to the other primary response genes studied (Fig. 3f), peaking at 4 h and decreasing thereafter, making it unlikely that it is induced by IFNβ. After a significant Selleckchem BYL719 one-way ANOVA (F = 67.76, df 5, 25, p < 0.0001), Bonferroni post hoc tests showed that ME7 + poly I:C was significantly higher than NBH + poly I:C but ME7 + saline was not significantly different to NBH + poly I:C (p > 0.05). IBA-1, COX-2 and IL-1β staining illustrated clear morphological evidence of microglial activation (Fig. 4 a versus b and c) and increased expression of COX-2 (d and e) but an

absence of IL-1β-positive cells (g and h) in ME7 animals with respect to NBH controls 3 h after treatment with saline or poly I:C. IBA-1 revealed significantly increased numbers of activated microglia (p   < 0.001 ANOVA with Bonferroni post hoc test; Table 2) in ME7 animals compared to NBH with no further increase following administration of poly I:C (p≫0.05p≫0.05). Upon systemic challenge with poly I:C these microglial cells, in the periventricular and dentate gyrus regions, now synthesised detectable SGI-1776 nmr levels of IL-1β (i) in ME7 but not NBH animals. IL-1β positive cells were found to be significantly higher in number in ME7 animals challenged with poly I:C than all other groups (p < 0.05 by ANOVA with Bonferroni post hoc test; Table 2). The endothelial cell layer was also induced to synthesize COX-2 in response to systemic poly I:C in both NBH and ME7 animals (d and f). Quantification of individual COX-2-labelled cells is not straightforward in the tightly apposed endothelial layer of hippocampal vessels, but it is clear that the vast majority of hippocampal

vessels are positively labelled after poly I:C challenge in NBH and ME7, while those in the ME7 + saline group are not. Numerous cells in periventricular and perivascular areas and around the dentate gyrus showed IRF3 labelling, and there was evidence of more intense PIK3C2G and more frequent staining of nuclei in the hippocampus and thalamus, consistent with nuclear translocation in the areas of prior ME7-associated pathology. There were no gross changes in the hippocampal levels of PrPSc in response to systemic poly I:C challenge ( Supplementary data). Fig. 5(a–d) shows evidence of increased IFNα/β action in the hippocampus via expression of IRF7, OAS, PKR and Mx1 transcription. These genes are known to be IFNβ-responsive, STAT1/2-dependent genes and are not induced directly by TLR3 signalling or by IRF3 activation (Honda and Taniguchi, 2006). IRF7 was clearly induced by poly I:C (main effect of poly I:C: F = 231.16, df 1, 14, p < 0.0001). There was also a main effect of disease (F = 39.

Quantification of the rhythm disturbances (ASI) revealed that recombinant PhKv significantly decreased the duration of arrhythmias in 47.5% (3.8 ± 0.9 vs. 8.0 ± 1.2 in control group). When compared to the native toxin, the recombinant PhKv had similar effectiveness

in decreasing the duration of arrhythmias in isolated rat hearts ( Fig. 2B). Altogether, FDA-approved Drug Library order these results indicate that native and recombinant PhKv possess an antiarrhythmogenic effect. In an attempt to investigate the mechanism underlying the antiarrhythmogenic effect of PhKv, we evaluated the action of this toxin on heart rate of isolated perfused rat hearts. Fig. 3 shows that perfusion of hearts with 240 nM PhKv induced a significant reduction in heart rate. This effect was partially blocked by pre-treatment with atropine and potentiated by pyridostigmine, suggesting that, at least in part, the antiarrhythmogenic effect of PhKv was mediated by a reduction in heart rate caused by release of acetylcholine (Fig. 3). In addition, in vivo ECG recordings reveled that PhKv reduced the HR and increased the RR, PR and QT intervals ( Fig. 4). SCH727965 purchase To test directly if PhKv enhances release of acetylcholine, we measured spontaneous and evoked release from motor nerve terminals innervating diaphragm neuromuscular junctions. Recordings were made under controlled

conditions and then in the presence of toxin in the same fiber, thus each synapse served as its own control. The toxin PhKv (200 nM, 10 min) caused a 2.18 ± 0.48 – fold increase in the frequency of spontaneous miniature endplate potentials (n = 4, Fig. 5). Since it was necessary to stop bath perfusion during

toxin CYTH4 application, we performed time-matched control experiments without a toxin. These experiments showed no significant increase in MEPP frequency (relative MEPP frequency after 10 min was 0.88 ± 0.12, n = 4). In contrast to the increased rate of miniature endplate potentials, we observed no change in quantal size or the quantal content or kinetics of evoked endplate potentials. We conclude that PhKv increases spontaneous release of acetylcholine from motor nerve terminals. The lack of effect on evoked release suggested that PhKv may depolarize the nerve terminal without causing major alterations on the presynpatic action potential and the consequent influx of Ca2+ into the nerve terminal. It has been previously reported that PhKv can inhibit transient outward (A-type) K+ current in GH3 cells (Kushmerick et al., 1999), raising the possibility that PhKv antiarrhythmic effects could be mediated by direct effect on cardiomyocyte electrical properties. In order to address this possibility, we measured action potentials and Ca2+ transient parameters in freshly isolated ventricular myocytes exposed to 250 nM PhKv for 10 min. As shown in Fig. 6A and B, PhKv had no effect on ventricular myocyte action potential nor Ca2+ transient parameters.

, 2005 and Precopio

et al., 2007). Ki67 is a nuclear protein that plays a role in the regulation of cell division. This marker has been used extensively in cancer biology to indicate tumour cell proliferation (Gerdes, 1990 and Scholzen and Gerdes, 2000). The protein is expressed during all active phases of cell division, but is absent in quiescent cells and during DNA repair (Gerdes et al., 1984). Intracellular Ki67 expression directly ex vivo, or after in vitro cell culture, has been used to measure specific T cell responses induced by vaccination ( Stubbe et al., 2006, Cellerai et al., 2007 and Miller et al., 2008), or turnover of these cells in individuals with chronic viral infections, such as HIV infection ( Sachsenberg et al., 1998 and Doisne et al., 2004). In this study, we show that Ki67 expression in T cells is a specific and quantitative indicator of proliferation, and

that results ALK inhibitor are comparable to those when proliferation is measured by other methods. We also show that measurement of Ki67 may be applied to longitudinal monitoring of vaccine-specific T cell responses. Overall, the Ki67 assay offers a reliable, versatile and simple method for detection of antigen-specific T cell proliferation. cancer metabolism inhibitor Healthy adult donors were recruited at the Institute of Infectious Disease and Molecular Medicine, University of Cape Town. Healthy, 18 month old toddlers were recruited at the South African Tuberculosis Vaccine Initiative clinic sites in the Western Cape, South Africa, before, and 11–13 days after their routine 18 month vaccination with TT. Enrolled toddlers had received all routine childhood vaccinations as set out by the WHO Expanded Programme on Immunisation. Heparinised venous blood from adults and toddlers was collected into BD Vacutainer CPT tubes (BD Biosciences)

and immediately processed as outlined below. Participation of all participants was in accordance with the Declaration of Helsinki, the US Department of Health and Human Services guidelines, Depsipeptide and good clinical practice guidelines. This included protocol approval by the Research Ethics Committee of the University of Cape Town, and written informed consent by all adults or parents of the toddlers. Whole blood (125 μL diluted 1:10 in warm RPMI 1640) was incubated with antigens for 6 days at 37 °C with 5% CO2. Antigens were used at the following final concentrations: 1 × 105 cfu/mL Danish BCG (Danish strain 1331; Statens Serum Institut), 1 μg/mL TB10.4 protein (kindly provided by Tom Ottenhoff, Leiden University, Leiden, Netherlands), 2 μg/mL M. tuberculosis purified protein derivative (PPD, Statens Serum Institut) and 0.16 IU TT (Tetavax, Sanofi Pasteur). On day 6 (day 3 for PHA), 10 μmol/L BrdU (Sigma-Aldrich) was added for the last 5 h of culture. When intracellular cytokine expression was assessed, 10 ng/mL phorbol 12-myristate 13-acetate (PMA, Sigma-Aldrich), 1.5 μg/mL ionomycin (Sigma-Aldrich) and 1.

Tristemente esquecidas estão as meninas sequestradas pelo Boko Haram, as mutiladas em nome da estupidez da crença, as cruelmente torturadas pelas guerras, as violentadas cotidianamente nas nossas cidades, as que morrem ou têm suas vidas devastadas pela violência de

gênero ou pelo descaso do Estado. Para todas elas e para todos nós, resta o pensamento do escritor anglicano John Donne, que em 1764 afirmava: “Nunca procure click here saber por quem os sinos dobram, eles dobram por ti”. “
“O envelhecimento ovariano feminino é um processo contínuo que se inicia no nascimento e se estende até o período da menopausa. O mecanismo principal do envelhecimento é o learn more esgotamento do pool folicular que ocorre de forma progressiva e contínua. A idade da mulher é fator importante que determina o declínio da fertilidade, que se inicia após os 35 anos. Esse declínio é acompanhado de mudanças como a redução da fertilidade, o aumento das taxas de aneuploidia, a irregularidade do ciclo menstrual e, finalmente, a menopausa. 1 Com o passar dos anos, a fecundidade feminina diminui como consequência da perda quantitativa dos folículos ovarianos e da redução da qualidade oocitária. Essa redução está associada

ao aumento da incidência de abortos e aberrações cromossômicas.2 O número de folículos ovarianos diminui em ritmo exponencial: a taxa de perda folicular mais do que dobra quando os números caem abaixo do nível crítico de 25.000 folículos, por volta dos 37 anos.3 O período de perimenopausa é caracterizado pelo aumento da irregularidade menstrual. A transição de perimenopausa para a menopausa é estabelecida quando os ovários apresentam

cerca de 1.000 folículos e ocorre em média aos 51 anos.4 Apesar disso, estudos epidemiológicos mostram que 10% das mulheres na população em geral atingem a menopausa antes dos 45 anos e cerca de 1% antes dos NADPH-cytochrome-c2 reductase 40 anos. Em média a fertilidade começa a diminuir 13 anos antes do início da menopausa, ou seja, uma em cada 10 mulheres terá redução da fertilidade aproximadamente aos 32 anos.1, 2, 3, 4 and 5 Portanto, 10% das mulheres podem estar em risco de baixa fecundidade durante a terceira década de vida e apresentar má resposta à estimulação ovariana.5 O FSH foi a primeira ferramenta de avaliação da reserva ovariana e rotineiramente era usada como diagnóstico propedêutico de casais inférteis.6 Os níveis de FSH começam a aumentar muito tempo antes do início da irregularidade do ciclo menstrual e continuam a subir posteriormente.7 A contagem de folículos antrais (CFA) por meio de ultrassonografia transvaginal parece refletir o número de folículos primordiais remanescentes e pode ter confiável grau de correlação com outros marcadores bioquímicos, especialmente o hormônio anti‐Mülleriano (AMH).

Thus, if the (only) observed positivity is a P3, the question then becomes: where is the P600? If the present late positivity is a P3, the lack of a distinct P600 entails that there is no P600 as a general, necessary consequence

of syntactic processing, or at the very least that it depends on specific (as of yet unspecified) aspects of the task. In either case, a model of the P600 as natural correlate of automatic syntactic processing must be amended. In addition, the assumption that the present buy Enzalutamide paradigm only elicited a P3 but no P600 is at odds with results demonstrating that the P600, in fact, has a stronger propensity to appear in task-relevant contexts than when task relevance and syntactic manipulation status do not coincide. As noted in the introduction section, the P600

– following both syntactic and semantic anomalies – is enhanced GSI-IX price by more explicit tasks (Hahne and Friederici, 2002, Haupt et al., 2008, Osterhout et al., 1996 and Osterhout et al., 2002). It is greatly attenuated and often absent (Batterink and Neville, 2013 and Hasting and Kotz, 2008; Royle, Drury, & Steinhauer, 2013) when subjects do not consciously attend to grammatical violations – in contrast to syntax-sensitive negativities, which often remain rather unaffected by task (e.g. Haupt et al., 2008). It also appears highly unlikely that the use of an immediate-response paradigm led to a higher likelihood for a P3 in this Erythromycin study as opposed to previous sentence processing experiments employing similar violation paradigms and delayed reaction. It has been established that the P3 follows the event affording decision making and response selection, not response execution. A direct comparison of immediate and delayed response tasks (e.g. Grent-‘t-Jong et al., 2011 and Praamstra et al., 1994) reveals that a P3 is always seen on the critical

stimulus itself, whether it is immediately followed by a response or not. In other words: the P3 does not “wait for the ‘go’ signal”. In accordance with these findings from non-linguistic paradigms, a P3 is expected following task-relevant violations in typical (delayed-response) EEG sentence processing experiments just as for the present immediate-response paradigm. Finally, it may be questioned if passive perception and comprehension is indeed the more “natural” mode of language processing, as opposed to “preparation for situated action” (Barsalou, 1999). In summary, when the present study is considered in light of the full range of existing data, there is no principled reason to assume that the paradigm employed here should have been more susceptible to eliciting a P3 effect than previous violation studies on sentence processing. The fact that the only positivity following the processing of structural information in our study is RT-aligned thus has implications for our understanding of the P600.

Activation of the complement cascade is essential for effective clearance of many pathogens, but when complement activity is improperly

regulated it can lead to extensive tissue damage. As early as 1988, complement deposition in synovial membranes of some patients with meniscal tears and cartilage degeneration was noted [15]. selleck chemicals llc Increased synovial complement component deposition in the setting of acute flare-ups of symptomatic OA has been demonstrated [54]. Blood or serum leaking into the joint under circumstances of injury likely provides a source of complement proteins in many patients, but chondrocytes and synovial macrophages may also actively produce complement components and inhibitors [12]. Using proteomic approaches, complement components and immunoglobulins have been identified in synovial fluids from OA patients [34] and

in vesicles released from osteoarthritic cartilage in vitro [86]. Several investigators have demonstrated that molecular components of the articular extracellular matrix may affect complement cascade activity. Fibromodulin [95], cartilage oligomeric matrix protein (COMP) [40], and osteoadherin [96] have been shown to activate the complement cascade, either the classical or alternative pathways. In contrast, other matrix components can act as complement inhibitors, such as the NC4 domain of Collagen Anti-diabetic Compound Library IX [50]. Exactly how complement deposition occurs in synovium and cartilage in the setting of OA, and the role of the complement cascade in OA pathogenesis remains to be determined.

In recent collaborative studies, mice with impaired ability to generate the MAC were partially protected from the development of OA, providing direct evidence for a role of the complement system in OA pathogenesis [111]. The potential pathway to complement activation in the OA joint is depicted in Fig. 3. Activation of pattern-recognition receptors and the complement cascade results in transcriptional activation of genes involved in the development of inflammation, most notably genes for soluble mediators such as cytokines and chemokines. These mediators may be produced by a variety of cell types, including macrophages, chondrocytes and synovial Bcl-w fibroblasts [51]. A broad spectrum of cytokines and chemokines are detectable in joint tissues and fluids, and may prove useful as markers of the synovial inflammatory response. These same mediators may also play a role in development of joint inflammation and cartilage matrix destruction typical of OA. Some specific examples will be discussed below. Since the identification of IL-1 as a synovial factor that is able to induce cartilage destruction in vitro [26], much progress has been made regarding this cytokine’s role in driving catabolic responses in chondrocytes.

Recreational fishers include anglers and spear-fishers whose catch exceeds the quantity of commercially caught fish for some species. For example, recreational catch of red snapper off Louisiana was estimated at about 698,000 pounds in 2009, compared to 695,000 pounds of commercial catch landed at Louisiana ports [30]. Fishing activity is heavy everywhere on the continental shelf, particularly in Cyclopamine price and around artificial structures and coral reefs/banks, as well as on soft bottom habitats by demersal fisheries trawlers. However, fish in the pelagic ecosystem were deemed to be under less pressure than in the benthic ecosystem; consequently, food (fish) was not selected as a highest-priority ES here. Linked to the

above is recreational fishing as a cultural service (i.e., in terms of the recreational enjoyment derived). This is considered ROCK inhibitor a highest-priority ES around artificial structures and both highly and lesser-protected banks, but not in relation to soft bottom habitats, which do not tend to attract sports fishermen. Pelagic fish, such as swordfish and mackerel, are not targeted by recreational anglers to the same degree as many of the demersal fish species. Hence, their value here is considered medium, as is the stress on such fish populations. Non-Use/Ethical Value—Iconic Species” is a highest-priority ES for cetaceans/turtles in all three regions of the study area. This reflects the value

people gain from knowing that such charismatic animals continue to exist, for their own personal satisfaction and for the benefit of future generations.

Cetaceans (i.e., marine mammals) and turtles move between the continental shelf, slope/rise and abyssal plain during their migration, feeding or breeding activities. There are Celastrol a total of 28 species of marine mammals and six species of turtles known to occur in the Gulf of Mexico. All 28 species of marine mammals are protected under the Marine Mammal Protection Act, and six are listed as endangered under the Endangered Species Act (sperm, sei, fin, blue, humpback and North Atlantic right whales). Out of the six species of sea turtles in the northwestern Gulf, all are either endangered (hawksbill, Kemp’s ridley, and leatherback) or threatened (green, loggerhead, and olive ridley). The ecosystem services “Food” and “Recreational Fishing” are considered to face high stress on all banks. This is because the volume of commercial and recreational fishing (hook and line fishing is allowed on all banks) places high demands on key fish populations. ‘Low stress’ is assigned to all other ecosystem services on coral reefs and high protection banks, based on the assessment that these benthic habitats are well protected by existing regulations which limit (or prohibit) activities such as certain oil and gas developments, the use of bottom-damaging fishing equipment (e.g., fishing spears) and the collection of bottom biota by recreational divers.