The total daily arsenic dose at the NOAEL for this population in Bangladesh was estimated using literature on water consumption rates and the contribution of iAs from food in this population. The uncertainty in the use of this dose for the U.S. population was subsequently considered in evaluating

a possible RfD. Chen et al. (2011) did not report water intake; however, surveys of water consumption rates in other rural areas of Bangladesh and in the nearby region of West Bengal, India, consistently report a direct drinking water intake rate of 3–3.5 L/day on average, with an indication that field laborers could drink twice this amount or more (Table 3). Because the staple diet in rural Bangladesh and West Bengal consists of rice, curries, and other dishes selleck screening library cooked in liquid, water added to foods

in cooking contributes substantially to the amount of water intake. Estimates of Rapamycin mouse water intake from cooking ranged from 1 to 3 L/day with one study reporting 6.7 L used in cooking (Table 3). This high amount did not include utensil washing, but was not specifically reported as consumed, and may be an overestimate. On the other hand, indirect water intake may be underestimated because water in cooked foods was considered only for major foods, some beverages made with water were not included (e.g., teas), and because foods clonidine are commonly cooked with excess water (Chowdhury et al., 2001 and Watanabe et al., 2004). The unique practice in Bangladesh and West Bengal of boiling rice in excess water, some of which is discarded, can still increase the arsenic content of rice by 10–35% over the expected concentration based solely on the water content of the cooked rice because some of the arsenic

in the excess water is retained in the rice (Bae et al., 2002 and Watanabe et al., 2004). Cooking of curries in Bangladesh likewise involves a substantial amount of water that is boiled down, concentrating the arsenic in the liquid (Watanabe et al., 2004). The equivalent volume of indirect water intake that contributes to arsenic exposure may be similar to that for direct intake of drinking water (i.e., 3 L/day) based on reported arsenic intake from rice cooking water (based on an increased arsenic concentration in cooked rice) which was slightly greater than arsenic intake from drinking water (Ohno et al., 2007). Conservative estimates of average long-term water intake rates were thus 3 L/day for drinking water with additional contribution of arsenic in water estimated to be 2 L of water per day from cooking foods (5 L/day total). Assuming a 100 μg/L water concentration, the daily arsenic intake from water in the Araihazar district would be 500 μg/day (Table 4). The staple diet of rice and vegetables in Bangladesh also contains increased levels of iAs (Smith et al.

, 1993, Abe et al., 1998, Nakano and Nagata, 2003, Davern

et al., 2008, te Velthuis et al., 2011 and Hoedemakers et al., 2012); many of the mAbs that we have produced against FLC do not bind FLC from up to a quarter of individual myeloma patients. The extent of FLC structural diversity is reflected in the LC gene structure. Thus, the κ immunoglobulin gene family contains 81 genes located on chromosome 2, of which, at least 40 functional genes are responsible for V region variability, giving rise to at least 4 major V region types (Vκ1, Vκ2, Vκ3, and Vκ4) (Sitnikova and Nei, 1998 and Davern et al., 2008). Further, there are 5 genes responsible for encoding the J region, and 1 constant region gene expressing 1 of 3 allotypic forms (κm1, κm2, κm3) ( Sitnikova and Nei, 1998, Davern et al., 2008 and Jefferis and Lefranc, 2009). The λ immunoglobulin gene family appears to Epacadostat mouse support more diversity, in that there are at least 40 functional genes responsible for V region variability that results in at least 5 major V region types (Vλ1, Vλ2, Vλ3, Vλ6, and Vλ8). Further, there are at least 5 genes responsible for encoding the J region, and up to 7 genes for the C PD-0332991 cell line region that gives rise to at least 3 C region isotypes (Cλ1, Cλ2/3, Cλ7) ( Solomon and Weiss, 1995 and Davern et al., 2008). FLC diversity is extended by somatic mutations in the encoding

genes and post-translational modifications of FLC. Given this multiplicity of human FLC structures, it is not surprising that it is difficult to produce mAbs that would detect the FLC from substantially all patients and neoplastic plasma cell clones. To be clinically reliable any new assay for FLC should be tested against a large number of serum and urine samples to show that the mAbs are at least close to the ideal of detecting FLC from all

patients and neoplastic plasma cell clones. In plasma samples containing SPTLC1 normal polyclonal FLC, obtained from healthy donors, each of the mAbs provided similar quantitation of absolute FLC levels. These samples were obtained from UK blood donors, which include persons up to the age of 65 years. It is likely that some of these donors had MGUS, and indeed, one donor found to have an abnormal FLC ratio detected by both the mAb assay and Freelite™, had a 30 g/L IgG λ paraprotein. Similarly, we cannot exclude the possibility that some donors had a degree of renal impairment. For both polyclonal and monoclonal λ FLC in a thousand consecutive serum samples, the two anti-λ FLC mAbs exhibited excellent correlations with each other, and displayed good clinical concordance with Freelite™. The diversity in FLC repertoire may explain the more divergent correlations demonstrated in this study between the mAb assay and Freelite™ for highly elevated monoclonal λ FLC paraproteins (see Fig. 4).

A completely automated model selection procedure resulted in two quite different models, depending on the severity score cutoff that

was used to define response. Assuming that a response is given by a score of 2 or greater on the Southall scale, the model selected by an automated stepwise procedure was (Model 1): equation(Model 1) Response2∼Year+CAR+COL+TUG+Month+Age+RL_rms,Response2∼Year+CAR+COL+TUG+Month+Age+RL_rms, Estimate Std. error z Value Pr(>|z|) (Intercept) 699.74410 324.52124 2.156 0.0311* Year −0.34602 0.15989 −2.164 0.0305* CAR −10.30153 5.23157 −1.969 0.0489* COL −6.09617 3.02291 −2.017 0.0437* TUG −9.54309 R428 datasheet 4.89167 −1.951 0.0511. Month −3.04004 1.62113 −1.875 0.0608. Age 0.06393 0.02682 2.383 0.0172* RL_rms 0.18178 0.11832 1.536 0.1244 Signif. codes: 0‘***’ 0.001 ‘**’ 0.01 ‘*’ 0.05 ‘.’ 0.1

‘ ’ 1 Binomial models are somewhat difficult to interpret with respect to explanatory power, and the usual R summaries for binomial GLMs do not contain the kind of R-squared summary statistics one normally expects in a regression. There is a tool1 (“binomTools”) to extract information from binomial models to give an idea about their explanatory power. We used function Rsq in package binomTools to illustrate, roughly, how much explanatory power each model had, and to assess GSK2118436 datasheet how much additional explanatory power the various models had when including or excluding information on received level. We found that Model 1 had an R-squared value of approximately 0.58. We reran all models with the cutoff for scoring a response set this time to ⩾3 on the Southall scale. In this case, both forward and backward stepwise model selection indicated that the preferred model was [Model 2]: equation(Model 2) Response3∼Sex+N-other-boats,Response3∼Sex+N-other-boats,which means that a killer whale’s response to the passage

of a ship (using a severity score of ⩾3 as a cutoff), on average, was best explained by the number of small vessels in the area and the sex of the whale. Using strictly automated procedures, Model 2 did not include information on received noise level at the whale. Because a central focus of this study is to understand Ponatinib molecular weight whether noise was a better predictor of behavior than other variables, we compared the selected model (Model 2) to one that also contained information on received noise level. We found that equation(Model 3) Response3∼Sex+N-other-boats+RL-rms,Response3∼Sex+N-other-boats+RL-rms,had similar support from the data as Model 2. The difference between Model 2 and Model 3 was ΔAIC = 1.41, which means that there is no strong statistical support for dropping noise level from the model. On the contrary, explanatory power of the model increased from R-squared = 0.23–0.25 when we included a term for RL. We therefore proceeded on the grounds of management interest, and used Model 3 for interpretation. Estimate Std. error z Value Pr(>|z|) (Intercept) −8.54322 465.47010 −0.018 0.9854 SexM −1.54243 0.62471 −2.469 0.

The longitudinal changes in these histopathologic end points were compared against changes in prominent optical parameters as shown in Figure 8, C and D. In the treated group, a major shift in both histology and optical end points was seen, whereas minimal changes were observed across all of these parameters in the control group. In this study, a combination of DRS and AFS was used to investigate cisplatin-induced changes in tumor physiology and morphology across a period of 1 week in a mouse model for

ALK activation hereditary breast cancer. The changes in optical end points were compared against the degree of pathologic response. The results showed that various DRS and AFS parameters in the treated animals significantly changed throughout the course of treatment relative to the untreated animals. These parameters were the Mie-scattering slope (P < .0001), Mie-to-total scattering fraction (P < .001),

tissue oxygenation (P = .035), fat volume fraction (P < .0001), and fluorescence residual (P < .018). Ipilimumab Furthermore, the observed changes appeared to be proportional to the degree of vital tumor tissue and the formation of fibrosis. Optical scattering characteristics are dependent on the size and density of cell nuclei and organelles as well as on the composition of the extracellular matrix (e.g., macromolecular aggregates and collagen fibers). In the histopathologic evaluation, considerable alterations in the extracellular matrix (formation of fibrosis) and in the size and the density of (sub) cellular structures were observed in the tumors of the treated animals. These morphologic and structural changes may lead to changes in tissue-scattering

properties that in turn may translate into changes in the Mie-scattering slope and Mie-to-total scattering fraction. Although significant fibrosis and cellular disintegration after treatment with cisplatin may explain these specific changes, further research is needed to provide a better understanding of these relationships. Tumor tissue oxygenation values of untreated animals remained hypoxic over time, whereas tumors of treated animals became progressively more oxygenated. This is consistent with Montelukast Sodium previously reported results where improved oxygenation of tumor tissue was observed due to tumor regression and altered metabolism after treatment with doxorubicin [27], [43] and [44]. For example, Vishwanath et al. performed DRS using a surface probe and showed that mammary-tumor tissue oxygenation in treated mice increased after doxorubicin administration relative to the untreated controls. A particularly interesting finding was the additional fluorescence observed in the treated group. On the basis of two-photon imaging, the extra fluorescence was specifically found in the cellular components of tumor tissue treated with cisplatin. Fluorescence was tumor specific and not observed in liver or muscle tissue of the treated animals.

Similarly, the motor protein dynein (DynII2a) was also much lower in N36 barramundi than in N22. The expression of these related genes suggests that in response to rearing at 22 °C, extensive remodeling of the cytoskeletal elements is necessary towards the adaptation of barramundi to cooler conditions, or that lower temperatures are damaging to these molecules and that new cytoskeletal proteins are required to replace them ( Buckley et al., 2006). Osmotic stress in cells is known to induce remodeling of the cytoskeleton in order to modify cell volume and cytoskeletal proteins have previously been shown to be regulated

in teleosts in response to temperature stress ( Ju et al., 2002, Podrabsky and Somero, 2004 and Sarmiento et al., 2000). Both of the above mentioned theories are credited by the expression GSK2118436 in vitro of the “response to stress”

genes, namely heat shock protein alpha crystalline related b2 (Hspb2) and heat shock 70.3 kDa protein like (Hsp70.3), which were both shown to exhibit lower expression check details in N36 barramundi compared with N22 ( Fig. 3). Small heat shock proteins (such as Hspb2) are known to play important roles in the prevention of diseased states and in promoting resistance to environmental stressors. In Danio rerio, small heat shock proteins have been shown to express during embryonic development and in response to mild heat shocks ( Elicker and Hutson, 2007). Small heat shock proteins have also been thought to protect cytoskeletal proteins in the muscle ( Nakagawa et al., 2001) while the larger Hsp70.3 is a known responder to temperature stress with a particular focus on molecular chaperoning ( Buckley et al., 2006). The expression Hydroxychloroquine manufacturer pattern of both heat shock proteins (Hsp’s) fits with the proposed theory that an increase in microtubule genes (Tubb4b, Tubb2b and Tuba) and the motor protein DynnII2a demonstrates an adaptive response in northern barramundi towards coping

with cooler temperatures through some form of cytoskeletal remodeling. Through an analysis of genes from the “endopeptidase inhibitor activity” GO category, 3 complement component genes; complement component 3-like isoform 1 precursor (C3 9 of 9), complement component 3-like precursor (C3 8 of 9) and predicted compliment C3 (C3 2 of 9), all showed a significant decrease in expression within southern barramundi reared at 36 °C in comparison to northern barramundi reared at 36 °C. In fish, the complement system is one of the main immune responses and causes lysis of target cells and the activation of phagocytosis (Boshra et al., 2006, Claire et al., 2002 and Tort et al., 2004). The depression of all three C3 related genes is suggestive of an immune suppression in cool adapted southern fish exposed to warmer rearing temperatures in comparison to warm adapted northern fish.

The i.c.v. injection of 4-AP had no effect ABT-199 in vivo on memory, but induced shaking, circling and tonic–clonic seizures at the higher doses tested. In fact, clinical trials have shown that although 4-AP improves cognitive functions in AD patients, the incidence of adverse-effects has hindered its clinical use (Davidson et al., 1988 and Wiseman and Jarvik, 1991). Interestingly, the analysis of amino acid sequence of Tx3-1 shows no relation to other K+ channel blockers (Cordeiro et al., 1993).

The lack of homology with other known blockers of K+ channels could explain the selective pattern of toxin against IA currents, and thus a possible better therapeutic profile when compared to the non-selective Kv blocker 4-AP. In vitro experiments shed light on the involvement of IA currents in AD’s cognitive decline ( Kerrigan et al., 2008, Pan et al., 2004 and Plant et al., 2006). The Aβ peptide, which accumulates in the brain of AD patients ( Fraser et al., 1997; Prince et al., 2009), alters synaptic plasticity ( Holscher www.selleckchem.com/products/MLN-2238.html et al., 2007 and Cheng et al., 2009), and ion channel function, such as potassium (K+) channels ( Furukawa et al., 1996). Moreover, current evidences suggest a role for Aβ peptides in IA K+ currents regulation ( Kerrigan et al., 2008, Pan

et al., 2004 and Plant et al., 2006). Therefore, we evaluated whether Tx3-1 alter Aβ25-35-induced memory deficits in mice. Administration of Tx3-1, immediately after training session, reversed the Aβ25-35-induced memory impairment. Interestingly, Tx3-1 proved to be more potent in Aβ25-35-treated mice when compared to the control group. One of the causes of this better effect could be attributed to the enhanced expression of cortical and hippocampal IA K+ channels induced by Aβ25-35 ( Pan et al., 2004). The higher potency of Tx3-1 in AD-like conditions makes this toxin a potential prototype for the emergence of more effective therapies

for AD-related cognitive decline. In line with this view, Tx3-1 has been produced through bacterial expression system ( Carneiro et al., 2002). This molecular biological technique is useful to produce not only the recombinant toxin but also to generate mutated versions of the native peptide. Here we reported the memory enhancing effect of Tx3-1, a selective IA blocker, in physiological next and AD-like conditions in mice. Despite the data showed here, more experiments, such as electrophysiological techniques, are needed to better elucidate the effect of Tx3-1 on neuronal mechanisms involved in memory storage. This study was supported by Conselho Nacional de Desenvolvimento Científico (CNPq, Brazil – 306164/2010-8, 481664/2010-6, 476551/2009-9), Toxinologia – Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (Capes 2865/2010, 1444/2011), Instituto Nacional de Ciência e Tecnologia (INCT) em Medicina Molecular (MCT/CNPq) and FAPEMIG. We thank CNPq, CAPES and FAPEMIG for the fellowship support.

5% of the contigs (Table 2). These data generated from the mantle of P. maximus form a valuable addition to those generated from hemocytes of the same species ( Pauletto et al., 2014) and, in a

more general context, to the transcriptomes generated for other molluscs including the Yesso scallop Patinopecten yessoensis ( Hou et al., 2011), Mytilus galloprovincialis ( Craft et al., 2010), Laternula elliptica ( Clark et al., 2010), Meretrix UK-371804 meretrix ( Huan et al., 2012), Ruditapes philippinarum ( Milan et al., 2011), Haliotis midae ( Franchini et al., 2011), several pearl oysters ( Huang et al., 2013) and the oyster genome data ( Zhang et al., 2012), thus increasing the sequence resource available for commercially important shellfish species and for researchers investigating shell deposition processes in molluscs. The sequence data for this transcriptome has been deposited in the GenBank SRA, accession number: SRP040427. The contigs, and the annotation for those contigs with a match of 1e − 10 and lower, are available from http://ramadda.nerc-bas.ac.uk/repository/entry/show/Polar+Data+Centre/NERC-BAS+Datasets/Genomics/. This study was funded by grants from the Région Bretagne, i.e. the

Pemadapt project (ref. 6368) and a doctoral fellowship to S.A. (Protmar project, ref. 6197). This study was also supported by a Natural Environment Research Council (NERC) grant to Lloyd Peck (NE/G018) and the British Antarctic Survey Polar Sciences for Planet Earth programme, which is also funded by the Natural Environment Research Council. Two French National Research Agency Selleckchem NU7441 (ANR) programmes also supported our research: COMANCHE (ANR-2010-STRA-010) and LabexMER (ANR-10-LABX-19-01). “
“Three congeners of the salmonid fish family with high commercial value were under study Lenvatinib research buy to identify species-specific markers for a validated species determination: Oncorhynchus mykiss, Salmo salar and Salmo trutta. The latter ones are common in Polish marine waters, whereas O. mykiss is only represented in this region in hatcheries. Difficulties in species identification may result in non-sustainable

salmon fisheries leading to imbalances in the ecosystem. The development of easy tests by means of molecular markers will therefore help in monitoring fishery activities as well as natural stock development. Single nucleotide polymorphisms (SNPs) have been used for ecological and conservational studies and have proven very useful for differentiating individuals, populations and species. A species-specific SNP-microarray initially comprised of 15163 loci was constructed and then optimized to 7000 markers for functional genes of S. salar in CIGENE, Norway. It has been used in studies of differences between farmed and wild Atlantic salmon ( Karlsson et al., 2011), genetic architecture of North Atlantic populations ( Bourret et al., 2013), and characterization of SNPs in S. trutta populations from the Southern Baltic Sea ( Drywa et al., 2013).

One review analyzed the cumulative experience with IFN-alpha in 279 patients with PV from 16 studies.52 Overall responses were 50% for reduction of hematocrit to less than 0.45% without concomitant phlebotomies, 77% for reduction in spleen size and 75% for reduction of pruritus. In a review article, Silver updated his experience on the long term use (median: 13 years) of IFN-alpha in 55 patients with PV.53 Complete

responses, defined by phlebotomy free, hematocrit less than 45% and platelet number below 600 × 109/L, were reached in the great majority of cases after 1–2 years of treatment and the maintenance dose could be decreased in half of the patients. Noteworthy is the absence of thrombohemorrhagic events Target Selective Inhibitor Library clinical trial during this long follow-up. IFN-alpha has been also used in ET patients. The results of several cohort studies, reviewed in Lengfelder et al.54 indicate that reduction of platelet

count below 600 × 109/L can be obtained in about 90% of cases after about 3 months with an average dose of 3 million IU daily. IFN-alpha is not known to be teratogenic and does not cross the placenta. Thus, it has been used successfully throughout pregnancy in some ET patients Natural Product Library clinical trial with no adverse fetal or maternal outcome. The main problem with IFN-alpha therapy, apart from its costs and parental route of administration, is the incidence of side effects. Fever and flu-like symptoms are experienced by most patients 4-Aminobutyrate aminotransferase and usually require treatment with paracetamol. Signs of chronic IFN-alpha toxicity, such as weakness, myalgia, weight and hair loss, and severe depression, limit its long term use. Pegylated forms of IFN-alpha allow weekly administration, potentially improving compliance and possibly providing more effective therapy. A phase 2 study has shown that following pegylated interferon

alpha-2a therapy the malignant clone as quantitated by the percentage of the mutated allele JAK2V617F was reduced.55 More limited effects on JAK2 mutational status have been reported after therapy with pegylated interferon-alpha 2b in a small group of patients with PV and ET.56 Kiladjian et al.57 performed a prospective sequential quantitative evaluation of the percentage of mutated JAK2 allele (%V617F) by real-time polymerase chain reaction (PCR) in patients treated with pegylated interferon-alpha-2a. The %V617F was decreased in 26 (89.6%) of 29 treated patients from a mean of 45% to a mean of 22.5% after 12 months of treatment, with no evidence for a plateau being achieved. In two patients, JAK2V617F was no longer detectable after 12 months, such complete molecular response being observed in a total of 7 patients (24%) at time of last analysis after a median follow-up of 31 months. These impressive results have been confirmed by the M.D. Anderson Cancer Center investigators.

Adjusted ORs for each exposure of interest were calculated with conditional logistic regression adjusting for all exposures in addition to age, PPI use, and previous

gastrointestinal procedures. As calendar year, sex, and primary care practice were precisely Trametinib price matched on in the controls, it was not necessary to include them in the model. Comorbidity was added last, and its association with bleeding tested using a likelihood ratio test. The variance inflation factor (a measure of the increase in model variance due to correlation between variables) was calculated for each exposure of interest to assess the effect of correlation between variables. All exposures with a variance inflation factor >5 were excluded from the final conditional logistic regression model.18 The final model was then stratified into cases with a recording of peptic ulcer and those without. Sequential (or extra) population attributable fractions (PAFs) were calculated for each exposure, using the prevalence among the cases and the respective coefficients from the conditional logistic regression model.19 Sequential PAFs differ from the standard

adjusted PAFs that are usually presented. They are calculated Omipalisib by estimating the additional proportion of cases attributable to each exposure, after removing the proportion of cases already attributed to the combined effect of all other exposures in the Olopatadine model. The final model was then stratified into cases with a recording of peptic ulcer and those without. All analysis was performed using Stata software, version 12 (StataCorp LP, College Station, TX). Previous studies of risk factor medications, such as NSAIDs,20 have been conducted in study populations that excluded patients with known risk factors for GIB.

To allow comparisons with these, we re-estimated the crude ORs for each of the risk factor medications after excluding any cases and their controls with nonmedication bleed risk factors. To assess the effect of the choice of the exposure exclusion time window before the bleed event on the effect of NSAIDs, we also re-estimated a model that included NSAID use up to 30 days before the index date. Two additional sensitivity analyses were performed to assess the effect of potential under-reporting. First the analysis was restricted to those older than 65 years old and who were eligible for free prescriptions, to assess the effect of potential under-reporting of nonprescribed NSAID use. Secondly, multiple imputation was used to re-estimate the association with comorbidity by imputing missing values for alcohol and smoking status. Alcohol and smoking were categorised as binary exposures of excess alcohol or current smoking to fit the logistic regression imputation model.

Samples were placed on ice in the field, then later frozen. In the laboratory, mussels were measured for shell total length, thawed and dissected. Adductor muscle tissue was dissected from individual animals, rinsed in deionized water (DI), and dried at 60 °C. The outermost

10 mm of mussel shells that represented the most recent growth was broken off and treated with bleach to remove this website organic matter. Shells were soaked overnight in household bleach (Chlorox, 6% sodium hypochlorite) to remove soft tissues, crushed into coarse fragments and soaked again overnight with bleach, then rinsed extensively with DI prior to drying at 60 °C. Barnacles were thawed, basal diameters were measured, and for each station approximately 50–100 animals with basal diameters of 5–20 mm were separated from their shells and combined into a composite site sample. Soft tissues were placed briefly in 1 N HCl and any carbonate shell detected by

bubble evolution was removed under a dissecting microscope. Cleaned soft tissues were then rinsed with deionized water and dried at 60 °C. Barnacle shells were treated with bleach as described above for mussels. Barnacle soft tissues Pirfenidone molecular weight were pulverized with a steel rod in glass vials. All other samples including shells and tissues of mussels were pulverized with a Wig-L-Bug automated grinder (Dentsply International). Shells and tissues were analyzed for δ13C by standard combustion methods with isotope ratio mass spectrometry (Fry, 2007), and results are reported as δ13C values using the VPDB reference (Coplen, 1994) where δ13C = (RSAMPLE/RSTANDARD − 1) * 1000 and R = 13C/12C. Samples for radiocarbon analyses were sent to the Rafter Radiocarbon Laboratory in Lower Hutt, New Zealand for measurement with accelerator mass spectrometry; results are reported as Δ14C values ( Stuiver and fantofarone Polach, 1977). For

δ13C, both diet and inorganic carbon dynamics have been shown to affect filter feeder isotope values (Fry, 2002), with the inorganic carbon dynamics at the base of food webs leading to higher δ13C values for plants and animals in more marine portions of estuaries. To account for this basal or baseline effect which is conveniently recorded by inorganic carbon in shell carbonate, the fractionation between shells and filter feeder tissues was calculated as 13ε=(RSHELL/RTISSUE-1)*100013ε=(RSHELL/RTISSUE-1)*1000where R is the 13C/12C isotope ratio in the δ13C definition. The 13ɛ values can be thought of as the baseline-corrected fractionation through the food web leading to filter feeders, and can be compared to the fractionation expected for dietary reliance on 100% non-oil normal estuarine foods versus fractionation expected from a 100% oil-based diet.