, 2001 and Yeung et al., 2009). The monoclonal antibodies were generated to target respiratory syncytial virus (RSV) and would not be expected to bind to targets in the brain. A human mAb

was used to avoid potentially faster clearance of mouse mAb dosed to rats, and enable detection of the human Fc in rat tissues. Studies were 24 h or less to avoid differences in serum levels due to the relationship of FcRn binding affinity and circulating half-life. The two variants have been shown to have rat FcRn binding Apoptosis inhibitor affinities, of 77 nM for N434A and >1000 nM for H435A at pH 6.0 (Kliwinski et al., 2013). Both variants had identical pI values of 7.2. The circular dichroism (CD) spectra for both the near and far ultra-violet ranges showed very similar secondary and tertiary protein structure for both of the variants. They had the same Size Exclusion Chromatography (SEC) profiles with no covalent

aggregates, and were stable at 25 °C for 4 d. There was no interaction with mucins, which would confound their GSI-IX price delivery by intranasal route (data not shown). FcRn binding variants (H435A and N434A) were administered intranasally into each nostril of rats (40 nmol/rat) and plasma was collected after 20, 40, and 90 min post-dose. The levels of the FcRn binding variant increased to levels that reached ~200 ng/mL in the circulation at a greater rate than the non-FcRn binding variant (Fig. 1A). Rat brain hemispheres were collected after brain perfusion, at 20, 40, and 90 min post-dose from different rats. FcRn binding variants delivered into the brain (ng/g) were detected by an ELISA-based MSD assay that detects full-length mAb (Fig. 1B). N434A entered the brain at a faster rate than H435A and peaked at a higher level at 20 min. Despite the greater

degree of uptake of N434A, levels of this variant dropped to very low levels within the same 90 min timeframe many as H435A. Statistical comparison of the AUC values generated for each variant showed a statistically significant difference (N434A AUC 1637 ng min/g vs. H435A AUC 827 ng min/g, P<0.05), representing an approximately two-fold faster rate of efflux for N434A compared to H435A. To monitor that test article was correctly deposited with the tube insertion technique; olfactory epithelia from both nostrils were collected at 20, 40, and 90 min post-dose and analyzed for FcRn binding variants. The PK profiles of each are shown in Fig. 1C and D. In both epithelia, the N434A variant was cleared at a much faster rate than the H435A, and the AUC values for each were significantly different (left AUC H435A 2.2×107 ng min/g vs. left AUC N434A 1.4×107 ng min/g, P=0.01; right AUC H435A 2.6×107 ng min/g vs. right AUC N434A 1.6×107 ng min/g, P<0.01).

7 g/L sodium bicarbonate under an atmosphere of 5% CO2 at 37 °C with 95% humidity. Continuous cultures were maintained

by sub-culturing cells every 4 days at 2.2 × 106 cells/25 cm2 flasks by trypsination. HepG2 cells were plated in 96-multiwell culture plates at 1 × 105 cells per well. To study BPA induced cytotoxicity, 24 h after plating, the medium was discarded and fresh medium containing BPA at various concentrations (10–100 nM) was added. At different time points (0-72 h), cellular viability was determined by the MTT assay [22]. In order to determine the effective concentration of ADW that protects 50% (EC50) of the cells from damage induced by the toxicant, Selleck BMS 354825 cells were incubated with BPA for 0-72 h to induce significant cell death. Based on the dose–response curves of cell death protection by ADW against the BPA induced toxicity

in HepG2 cells, the EC50 concentration was determined and used in the experiments to evaluate the protective potential of the ADW on several cellular parameters. Oxygen consumption rate assay kit was used to measure the oxygen consumption rate of the mitochondria in HepG2 cells according to manufacturer’s instruction (Cayman). Briefly, HepG2 cells were plated in 96-multiwell black culture plates at 1 × 105 cells per well and incubated overnight. The spent culture see more medium was removed from all wells and replaced with 150 μl of fresh medium with or without test compound along with experimental controls. The readings were recorded using (BioTek, KC-4) plate on fluorometric mode by following the kinetics of the reaction at excitation 380 nm and emission 650 nm for 200 mins with 1 minute interval time. The cellular ATP concentration was measured using an ATP Colorimetric/Fluorometric Assay Kit (BioVi-sion). Cells (106) were lysed in 100 μl of ATP assay buffer, homogenized, and centrifuged (13,000 X g, 2 min, 4 °C) to pellet insoluble materials. The supernatants were NADPH-cytochrome-c2 reductase collected and added to 96-well plates (50 μl per well) along with 50 μl/well of

the reaction mixture (ATP probe, ATP Converter, Developer Mix in ATP assay buffer). The plates were incubated at room temperature for 30 min, while being protected from light and absorbance in the wells was measured at 570 nm using a micro-plate reader (BioTek–KC-4). The absorbance of the no-ATP control was subtracted from each reading. Mitochondrial membrane potential (ΔΨM) was assessed using the fluorescent potentiometric dye JC-1 as described previously [23] and [24]. Briefly, at 24 h after the BPA treatment with or without ADW extract HepG2 cells were harvested, washed twice with PBS, and centrifuged for 8 min at 4500 rpm at room temperature. Then the cells were suspended with JC-1 (5 μg/ml) in serum-free RPMI-1640 and incubated for 15 min at 37 °C. After staining, the cells were collected at room temperature and washed thrice with pre-warmed PBS.

The flow cytometry data were subjected to a Mann–Whitney rank sum test (SigmaStat,

version 3.10, Systat Software, Inc., Chicago, IL). The data were considered statistically different if p < 0.05. The data for GFP and αSMA were tested with a paired two-tailed Student's t-test, and a normal Student's t-test for differences between the wound tissue in skin and in mucoperiosteum. The data from the adjacent tissue in skin and mucoperiosteum were tested similarly. If the data were not normally distributed, a Wilcoxon signed rank test was performed for paired data, and a Mann–Whitney rank sum test for independent data. The HSP47 and CD68 data were only tested for differences between the wound tissue and the adjacent tissue in skin. The data were considered statistically significant when p < 0.025. The fraction of GFP-positive mononuclear cells in the blood of the donor rats and the transplanted rats was not significantly buy PF-562271 different (86 ± 2% and 69 ± 9% respectively, Fig. 1). This indicates a good take of the bone marrow graft. The histology of the mucoperiosteum www.selleckchem.com/products/Staurosporine.html and skin is shown in Fig.

2A. Both tissues have a keratinized epithelium overlaying the lamina propria (mucoperiosteum) and dermis (skin). The mucoperiosteal epithelium contains more cell layers than the epidermis. Skin dermis also contains hair follicles with the arrector pili muscles and sebaceous glands. Underneath the dermis lies the hypodermis with fat cells. Both types of wounds have a high cell density. In the skin wounds, no regenerated hair follicles are present, and the hypodermis is lost. Further, Fig. 2 shows representative examples of the immunostainings. In the wounded mucoperiosteum, more GFP-positive cells are present than in the adjacent tissue (Fig. 2B). In skin, the numbers in wounded and adjacent tissue are similar. Few GFP-positive cells were detected in the epithelia or in the hair follicles of the unwounded skin. In the mucoperiosteal

wounds, high numbers of myofibroblasts were present, whereas far less were present Rapamycin in the skin wounds (Fig. 2C). Only few of these were also GFP-positive. No myofibroblasts were detected in the adjacent tissues of the mucoperiosteum and the skin. Activated fibroblasts (HSP47-positive cells) were present in the wounds and adjacent tissues of both the mucoperiosteum and the skin (Fig. 2D). Activated fibroblasts were brightly stained in the wounds, whilst they were stained less intensely in the adjacent tissues. Only few of the activated fibroblasts were also GFP-positive. The number of macrophages was similar in the wounds and the adjacent tissues of the mucoperiosteum and the skin (Fig. 2E). A relatively large number of these cells were also GFP-positive. Fig. 3 shows the quantitative data of the immunostainings. The total fraction of GFP-positive cells (Fig. 3A) in the mucoperiosteal wounds (8.1 ± 5.1%) was significantly larger than in the adjacent tissue (0.7 ± 0.8%, p = 0.025).

g., Wixted, 2007). Some researchers like Donaldson (1996) and Dunn (2008), for example, have argued that evidence from Remember/Know judgments, Confidence judgments (e.g., ROC curves) and even Source judgments can be re-interpreted in terms of a single dimension of memory strength (i.e., without needing to appeal to qualitatively distinct processes of familiarity and recollection; see recent exchange in Trends in Cognitive Science, 2011, Issue 15). Moreover, the precise nature of the empirical dissociation – for example,

a single, double, or cross-over dissociation – has also been questioned, particularly in neuroimaging data where the mapping Vorinostat molecular weight between hemodynamic Ganetespib nmr measures and theoretical concepts like memory strength, for example, may be nonlinear ( Henson, 2006; Squire et al., 2007). Nonetheless, the popularity of the recollection/familiarity distinction is due largely to the convergence of empirical dissociations across a range of paradigms, most of which appear relatively easy to explain in terms of two distinct processes of recollection and familiarity. In a standard recognition memory paradigm, a series of items are presented in a Study phase (“studied” items), which participants then have to distinguish, when presented again in a later Test phase, from randomly intermixed “unstudied” items

that were not Non-specific serine/threonine protein kinase presented at Study. As elaborated in other articles in this special issue, recollection in this paradigm generally refers to retrieval (recall) of contextual information that was present at Study, but that is not present at Test. Examples of this contextual information include spatial location of an item, or other thoughts/associations prompted by that item (corresponding to “external” and “internal” “source” information respectively; Johnson et al., 1993). Conversely, familiarity generally refers to a unitary, acontextual signal associated with the test cue itself, owing for example to residual effects of its recent processing in the Study phase (though

may also have other causes; see below), which is attributed to the Study phase by the participant. One variant of the recognition memory paradigm that has been used to support the recollection/familiarity distinction was introduced by Jacoby and Whitehouse (1989). In the “masked” version of this paradigm, each item in the Test phase is preceded by a brief, masked stimulus, for which participants typically have little to no awareness (or at least, do not appear to spontaneously identify). When the masked stimulus (prime) matches the test item (target), for example corresponding to the same word just in a different letter case (see ahead to Fig. 1), participants are more likely to call the test item “old” (i.e.

Normally the two biopolymers used include a protein molecule and a polysaccharide molecule

(Jun-xia, Hai-yan, & Jian, 2011). Soy protein isolate (SPI) has been used with success in the microencapsulation of hydrolyzed casein by spray drying (Molina-Ortiz et al., 2009), of essential orange oil by complex coacervation (Jun-xia et al., 2011) and of fish oil by an enzymatic jellification process (Cho, Shim, & Park, 2003; Serna-Saldivar, Zorrilla, La Parra, Stagnitti, & Abril, 2006). Studies carried out by Kim and Morr (1996) indicated that SPI showed greater compatibility with gum Arabic than with other polymers. The microparticles produced by complex coacervation, despite the advantage of encapsulating large amounts see more of core material (85–90 g/100 g), present low mechanical Bortezomib research buy and heat resistance due to the ionic nature of the interactions between the wall

forming polymers, and thus it is necessary to strengthen the wall by reticulation, generally involving the protein, which can be done using chemical or enzymatic reticulating agents (Burgess & Ponsart, 1998). The enzyme transglutaminase (TG) is a protein reticulating agent permitted for use in foods. TG (E.C. 2.3.2.13) catalyzes acyl transfer reactions, forming intra and intermolecular cross links in proteins, peptides and primary amines mainly by covalent bonds between glutamine and lysine residues, and its efficiency in forming cross links depends on the molecular structure of the protein (Chambi & Grosso, 2006; Griffin, Casadio, & Bergamini, 2002). The objective

of the present work was to evaluate the influence of varying the concentrations of the wall materials (soy protein isolate and gum Arabic, SPI:GA), the ratio of the wall material to the core material and the concentration of the reticulating agent Ribociclib cost (TG) in the microencapsulation of omega-3 polyunsaturated fatty acid ethyl esters by complex coacervation using a central compound rotational design (CCRD), analyzing the results by response surface methodology (RSM) and Tukey test for comparison of means with the control trials. Fish oil ethyl ester – EE – (62 g EPA + DHA/100 g fish oil ethyl ester, Vital Atman, Uchoa, SP), soy protein isolate – SPI – (The Solae Company, Porto Alegre, RS, Brazil, 88 g protein/100 g SPI), Instatgum gum Arabic AA – GA – (Acácia Senegal – CNI Colloides Naturais Brasil Comercial Ltda, São Paulo, SP, Brazil), Transglutaminase Activa TG-S® – TG – (Ajinomoto, Limeira, SP, Brazil). In order to produce the multinucleated microcapsules by complex coacervation, the conditions were pre-determined in relation to the raw materials and process according to Table 1 (first seven columns). The processing parameters adapted from Jun-xia et al. (2011) are described in the following steps: 1.

Plasma markers would have the great advantages of reducing learn more the number of lumbar punctures currently necessary, making sample collection easier and less invasive, and increasing attendance at follow-up visits. In conclusion, great efforts have been made by the WHO, NGOs and research institutions over the last few decades to actively regulate the transmission of sleeping sickness and to reduce the number of cases. Alternative diagnostic tools to improve patient management have been proposed and some of them have shown very promising results, but further studies are

needed to introduce these new tools into clinical practice. The authors wish to thank the FINDTRYP consortium for its scientific assistance. The authors also check details thank Dr. Veerle Lejon and the Foundation for Innovative New Diagnostics

(FIND, http://www.finddiagnostics.org/) for having kindly provided the photos reproduced in Fig. 2. “
“Platelets are small anucleated cell fragments also called thrombocytes [1]. With a diameter of 2–4 μm, they are the smallest cellular components of the bloodstream. Although platelets do not contain a nucleus, they can alter their protein profile by splicing and translation of a limited batch of messenger ribonucleic acids (mRNA) inherited from their parent cell, the megakaryocyte [2], [3] and [4]. Megakaryocytes are highly specialized hematopoietic cells [5], which derive from hematopoietic stem cells. L-NAME HCl They become polyploid (4–64 N) through several cycles of endomitosis [6], [7] and [8]. In addition, a cytoplasmic maturation occurs involving the formation of a demarcation membrane system (DMS) and the accumulation of cytoplasmic proteins and secretory granules [6] and [9]. The DMS is supposed to function as a membrane reserve for pro-platelet formation and constitutes the open canalicular system in mature platelets [5].

Granule number increases with megakaryocyte maturation. With an average lifespan of 10 days before being phagocytosed by the spleen or the liver [10], approximately 1011 platelets must be produced every day (around 10% renewal) [8] to ensure an average concentration of 150–400 × 109 platelets/L [11]. Platelet production is mainly regulated by thrombopoietin. This humoral factor is produced in the liver and the kidneys, and stimulates the production of thrombocytes in bone marrow, from their hematopoietic cell of origin, the megakyryocyte [5] and [8]. Cell apoptosis is also involved in the regulation process since pro-platelets contain active caspase-3 and 9 and their production is decreased by anti-caspase agents [11] and [12]. Mature platelets have a large number of secretory granules. They also contain endoplasmic reticulum and Golgi, as well as translation machinery. In addition, a few mitochondria are also visible under electronic microscopy, together with glycogen particles and a large cytoskeleton [5].

A few in vitro studies showing the related role of Akt, PTEN, and AR in BCa suggest that AR lowers Akt activity and increases PTEN expression that in

turn decreases BCa cell proliferation [27] and [28]. Collectively, these studies suggest that PTEN-Akt is a complex signaling pathway, operated under multiple levels of feedback; AR pathway is known to be involved in this feedback loop and has been shown to downregulate Akt and upregulate PTEN expression. Unlike previous studies, we did not find any association between expression of pAkt and Trichostatin A clinical trial pPTEN with AR status. This suggests presence of mechanisms other than AR that might be responsible for regulating Akt/PTEN expression. However, we found that expression of AR was associated with significantly selleckchem longer OS in patients with pAkt-positive tumors, suggesting protective role of AR in these patients. We also found a survival advantage with only 7.1% deaths in patients with AR+/pPTEN+ tumors, whereas loss of expression of both markers was found to be associated with lower OS with 32% deaths. These

results suggest that AR-PTEN coexpression might be decreasing the cellular proliferation and increasing apoptosis (action mediated by pAkt), resulting in increased OS in the subset of patients with AR+/pPTEN+ tumors. Reportedly, patients with Akt+ and PTEN− tumors have been shown to exhibit worst survival; however, these patients were not stratified into AR-positive and AR-negative groups [31]. We stratified tumors in context of combined expression of pAkt and pPTEN and determined the impact of AR expression on survival in patients with pAkt+/pPTEN− tumors. We found that, in a subset of women with pAkt+/pPTEN− tumors, expression of AR conferred a survival advantage, whereas loss of AR reduced the survival. Our results suggest that AR, independent of its coexpression with pPTEN, could be negatively regulating Aspartate Akt-mediated proliferative effect as shown by survival advantage of 2 years in patients with AR+/pAkt+/pPTEN− tumors when compared with AR−/pAkt+/pPTEN− tumors. This did not reach to

statistical significance possibly due to low number of patients (n = 31) in this subset ( Figure 2D). The mechanism of these important observations where AR appears to negate the proliferative and antiapoptotic effect due to activation of Akt and loss of PTEN, respectively, warrants further study. In the current study, survival analysis was limited to patients who went through a follow-up of 5 years or more (n = 82). A distinctly better survival was observed not only in patients with AR expression for whom we had 5-year follow-up but also in patients whose follow-up was between 2 to 11 years (n = 200, data not shown). However, relatively small number of deaths (n = 16) restricted us to perform multivariable analysis.

Although disease enhancement after vaccination has been identified for some other diseases the negative vaccine effectiveness for the Shamir vaccine is probably an artefact (residual age-confounding and collinearity). The confidence intervals show the uncertainty in the modelled Shamir VE. It could be argued that outbreaks are cases of vaccine failure that do not represent typical vaccine performance. If so, vaccine effectiveness estimates

would be pessimistic. That said, findings were consistent with (a) vaccine matching r1-values which suggested a good match for the homologous TUR 11 vaccine and a poor match for the Shamir vaccine (see Section 2) and (b) the large number of outbreaks seen within the Turkish vaccination programme. VE for the TUR 11 vaccine is comparable with the 60%–85% vaccine selleck kinase inhibitor Icotinib efficacy that would

be expected for a 3PD50 vaccine [14] and is close to OIE batch release requirements where >70%–75% of vaccinated cattle must have a protective titre [13]. When comparing the Shamir and TUR 11 vaccines, differences in VE are consistent with differences in vaccine match r1-values. The closest we had to a direct comparison of the two vaccines was in Afyon-1 where 11 doses of Shamir vaccine were used in one village whilst TUR 11 vaccine was used in the other investigated village. The TUR 11 vaccine was approximately twice as effective with 3/11 (27%) affected in cattle vaccinated with the Shamir vaccine and 11/80 (14%) in the TUR 11 vaccinated cattle STK38 (see Table 2), however, this comparison was under-powered. TUR 11 vaccine performance varied, possibly due to variability in (1) field conditions, e.g. season, time since vaccination, coverage, husbandry, body condition, nutrition and other animal factors; (2) vaccine potency at point of production; or (3) vaccine delivery (e.g. cold chain or shelf life adherence). The reduction in VE with increasing time since vaccination was as expected, with protection due to the TUR 11 vaccine declining after 100 days. The Shamir VE

appeared to decline sooner (after 50 days) (Table 2). The findings differ to those from a PD50 challenge study. A high potency (>6PD50) Shamir vaccine held in the EU vaccine bank protected against clinical FMD when challenged with the Turkish FMD Asia-1 Sindh-08 field virus [15]. Differences in protection will partly reflect differences in potency as poor vaccine match may be overcome if high potency vaccines are used [16] and in the challenge study the vaccine used was likely to be much greater than 6PD50. Furthermore, in the challenge study, animals were assessed at time of peak immunity (21 days after vaccination), whereas in the VE study time between vaccination and challenge varied from one to five months. NSP serology is a sensitive method of detecting animals with significant systemic viral replication [17]. As this will correlate with virus shedding, NSP status is a suitable outcome for vaccine evaluation.

Thus chronicity of HIV infection does not preclude immune response to highly conserved epitopes. It is well known that epitopes restricted by few HLA class I alleles confer variable degrees of protection

during natural infection, underscoring the need to design a vaccine that elicits immune responses that are substantially better than those seen during natural infection. The identification of “Achilles’ heel” epitopes in this study is an important first step. The biggest challenge for HIV vaccine design is to identify epitopes restricted by other HLA class I and class II alleles and adopt new immunization strategies and adjuvants that may lead to an effective way to prime the T-cell immune responses of these individuals against conserved epitopes that would impart a substantial fitness cost on the virus and control or prevent infection. In summary, the challenges faced in HIV vaccine design necessitate Cyclopamine a balanced approach to epitope identification, combining computational tools with experimental strategies. selleck Our

step-by-step immunoinformatics approach has successfully screened large amounts of sequence data and defined epitopes that are likely to accelerate vaccine development. On the other hand, the experimental approach described here does highlight the need to further validate some of the in silico predictions, as a few of our candidates did not prove to be immunogenic in in vitro assays despite binding with high affinity to HLA-A2. The approach described here appears to be an effective means of further triaging sequences to distil the best vaccine immunogen candidates, particularly in terms of their conservation

over time, which would provide valuable information and strategies for groups developing multi-epitope, pan-HLA-reactive vaccines for HIV and other pathogens. In this paper, we have identified 38 highly conserved immunogenic T-cell epitopes. The combination of the remarkable conservation and high immunogenicity of these epitopes over time and space supports their potential inclusion TCL in a globally relevant HIV vaccine. Conflict of interest: Anne S. De Groot and William Martin are senior officers and majority shareholders at EpiVax, Inc., a privately owned vaccine design company located in Providence, Rhode Island, USA. Leonard Moise holds options in EpiVax, Inc. Anne S. De Groot is also the founder and CSO of GAIA Vaccine Foundation a not-for-profit that will distribute the GAIA HIV Vaccine to developing countries when it is completed. GAIA Vaccine Foundation also provides material and technical support to the Hope Center Clinic where the HIV subjects were recruited. Contributions of the authors: Ousmane A. Koita directed the research being performed at the Laboratory of Applied Molecular Biology, University of Bamako, Mali. Lauren Levitz, John Rozehnal, and Kotou Sangare performed the assays in Bamako and assisted with the reporting and interpretation of the results. Karamoko Tounkara, Sounkalo M.

The proportion of cells with loss of membrane integrity and fragmented DNA was determined by flow cytometry using a FACSCalibur equipment (Becton and Dickinson System, San Juan, California, USA), as previously described (Jaroszeski and Radcliff, 1999 and de Lima et al., 2007). ECV-304 cells were treated with FA for 24 h, than the slides were washed, fixed and stained with

oil red O as previously described (Pearse, 1960). The slides were examined by light microscopy at 510 nm (Carl Zeiss Vision, Munchen-Hallbergmoos, Germany). Images were taken at 20× magnification AZD6244 and a representative image is shown (Fig. 2 and Fig. 4C). Cells were treated with the FA for 30 min. After treatment, the cells were incubated with hydroethydine (1 μM) for 30 min at room temperature in the dark. Cells were visualized in a fluorescence microscope (Carl Zeiss Vision, Munchen-Hallbergmoos, Germany), using the 590/46 nm filter and analyzed by fluorescence intensity using the KS 300 software. For quantification of ROS production images were taken at 20× magnification from 10 random fields of view for each well and were analyzed by fluorescence intensity using the KS 300 software. Values of the areas were PTC124 purchase averaged to obtain the mean values. A representative

image is shown (Fig. 2 and Fig. 4D). Results are presented as means ± SEM of 6–9 determinations from 2 to 3 experiments. Statistical analysis was performed by using one-way ANOVA and Tukey’s test (Graph Pad Prism 5; Graph Pad software) as indicated. Erastin The level of significance was set at p < 0.05. Treatment with SA for 24 h decreased the proportion of viable cells by 18% at 150 μM, 9% at 200 μM and 11% at 250 μM, as compared to vehicle (Fig. 1A). The proportion of cells with DNA fragmentation was increased by 3-fold due to treatment with SA at 150 μM, by 3.5-fold at 200 μM and 4-fold at 250 μM for 24 h, as compared to vehicle (Fig. 1B). The treatment with SA at 150 and 200 μM for 24 h did not change the content of lipids but at 250 μM decreased it by 25% compared to

vehicle (Fig. 1C). ROS Production was increased by approximately 2-fold due to SA treatment either at 150, 200 and 250 μM, as compared to vehicle (Fig. 1D). Treatment with SA and the association with PUFA (ω-3 and ω-6) for 2 and 6 h did not alter the viability and the percentage of cells with DNA fragmentation compared to vehicle (data not shown). Treatment with SA for 24 h decreased the proportion of viable cells by 18% at 150 μM as compared to vehicle (Fig. 2A). The combination of SA with DHA at 100 μM decreased still further the proportion of viable cells by 19% as compared to SA. On the other hand, the association of SA with EPA at 50 and 100 μM increased the proportion of viable cells by 12% and 9%, respectively, compared to SA. ω-6 FA (LA and γA, at 50 and 100 μM) increased the proportion of viable cells in the presence of SA by 20% as compared to SA (Fig. 2A).