Excitation spectra of living phytoplankton characterize the pigme

Excitation spectra of living phytoplankton characterize the pigment composition of algal cells and energy transfer processes from accessory pigments to chlorophyll a (Chl a). Analyses of these spectra provide information about the spatial distribution of these pigments in different vertical and horizontal transects, and

enable the phytoplankton community situation in coastal and open-sea waters to be established. In order to study the trends of phytoplankton changes, quite a long time-series is needed. The spectrofluorometric studies are therefore being continued in order to determine the interannual variability and longer-term changes in the marine ecosystem of the archipelago (Cisek et al. 2010). The Fluo-imager M32 B flow-through spectrofluorometer measures visible Panobinostat light excitation spectra and can be applied Forskolin molecular weight to the fluorescent constituents of phytoplankton pigments. The excitation wavelength from 400 to 600 nm is scanned by the monochromator; emission is at 680 nm. The aim was to reveal the fluorescence of Chl a induced by accessory pigments. The Chl a fluorescence emission at 680 nm, observed at several excitation wavelengths

that are coincident with the accessory pigment absorption maximum, is treated as an indicator of the abundance of different phytoplankton pigments ( Poryvkina et al. 2000). The most important advantage of spectrofluorometric measurements is that the in vivo measurements of recent water samples on board ship and the data-processing are both carried out quite quickly. The concentration of absorbing

molecules can be calculated from the recorded excitation spectra of Chl a in seawater samples. The advantages and limitations of the application of fluorescence actively induced in living phytoplankton analysis are discussed. The focus is on making correct SPTLC1 predictions of pigment concentrations from fluorescence data. The results of the high resolution mapping of chlorophylls and phycobilins in the Nordic Seas during the summers of 2003 and 2006 are presented. Dynamic spatial maps of phytoplankton pigments were registered with a Fluo-Imager flow-through spectrofluorometer. Characteristic patterns of the phytoplankton distribution in the study area and their evolution in time are discussed. The schedule of the r/v ‘Oceania’ polar cruise included the Greenland and Iceland and Norwegian Seas, known as the Nordic Seas. Figure 1 shows a map of the stations where the optical and CTD measurements were carried out. Water samples were collected from the surface layer (from 0 to 0.5 m) using a special pail from on board ship. The samples were poured into the flow- through system of the Fluo-Imager that allows in vivo measurements of natural water, without prior sample preparation. Fluorescence excitation spectra of seawater samples were measured with a Fluo-Imager M32 B spectrofluorometer at one emission wavelength, 680 nm, at the halfwidth of the optical filter Δλ = 5 nm.

In order to maximize their jurisdiction offshore, coastal states

In order to maximize their jurisdiction offshore, coastal states are inclined to a broad and inclusive definition of marine scientific research. States

have debated, for example, whether collection of routine meteorological and oceanographic observations Alectinib by voluntary observing ships, floats, and gliders, and activities such as marine surveys and bio-prospecting, constitute MSR [23] In a response to an inquiry by the World Meteorological Organization on whether routine marine observations and data collected for sea state estimation, weather forecasts, and climate modeling constitute “marine scientific research,” the chairman of the Third United Nations Conference on the Law of the Sea responded that they lie outside the regime of MSR.21 The United States has relied in part on this opinion to express the same view.22 The use of marine migratory species as oceanographic platforms adds to this milieu of discord and debate over the role of the coastal state in the MSR regime. Marine animals can be tagged anywhere in the world, and later through natural movement and migration, they may end up in areas under coastal state jurisdiction. The Intergovernmental Oceanographic Commission has issued guidance on the use of floating buoys or PARP inhibitor gliders inside a

coastal state׳s EEZ as part of a program pursuant to an international marine science effort. The guidance permits states to require notification in certain circumstances. A state must be notified if the

deployed device “might” enter the EEZ of a participating state that has so requested notification “reasonably in advance of the expected entry of the float in the EEZ.”23 This guidance, however, does not control the use of marine animals as platforms to collect marine data; bio-logging is not analogous. The difference between the two is that marine species follow unpredictable courses driven by decisions made by the animals themselves, whereas drifting buoys and floating instruments are driven by predictable wind and currents, and their intended trajectories are often modeled ahead of deployments as part of the studies they ZD1839 support. Furthermore, deployed floats, gliders and drifters are also recoverable, whereas tags deployed on animals are not. Bio-logging is further differentiated from other marine data collection activities because the course, track, and behavior of specific tagged animals are largely unpredictable and, essentially unknowable, when instruments are deployed. This is especially true for archival tags deployed on marine animals that do not provide information about the movements of animals until they are recovered or are jettisoned from the animal.

We further reasoned that favoring the classification of positive

We further reasoned that favoring the classification of positive represented the appropriately conservative approach to the decision on primaquine therapy with regard to patient safety. At intermediate G6PD activities in our experiments, the subjectivity of reading was most apparent between 2.75 and 3.5 U/gHb (37%–51% of normal; see Fig 3, Fig 4 and Fig 5) with both positive and negative readings

being relatively frequent. Reading with the CSG as negative in this range proved less likely than with FST (odds ratio = 0.44; 95% confidence Selleck Anti-diabetic Compound Library interval = 0.20–0.95; P = 0.04). We viewed erring in favor patient safety in this range to be a likely advantage of CSG over FST, but acknowledge denying primaquine therapy buy Afatinib to

any patient who may safely receive it would also be a poor outcome. Improving specificity with the CSG could perhaps be achieved by the availability of a dummy cassette permanently exhibiting a color representing that occurring at an intermediate G6PD range, where less intense color should be considered positive and more intense color negative for deficiency. Such a simple device would help guide this difficult subjective decision by the reader. Female heterozygotes impose uncertainty with G6PD diagnostics and primaquine safety. G6PD activity in any given blood sample represents the consensus activity of the many individual RBCs present in the sample. The mosaicism of female heterozygotes for G6PD activity phenotype among RBCs complicates that representation and has implications for the primaquine go vs no go output of a G6DPD diagnostic device. A hypothetical example illustrates this problem: a female presents a consensus G6PD activity of 50% of normal, and thus, she may often test negative for G6PD deficiency despite up to one half of her RBCs perhaps being fully vulnerable to primaquine-induced hemolysis.31 The data illustrated in Fig 5 affirm this problem. Both the FST and CSG performed Resminostat erratically with >30% and <80% of RBCs being G6PD inhibited (by 1.0 mM CuCl). The proportion classified as negative at 50% of normal activity was approximately 50%. If the G6PD-deficient RBCs in such patients were indeed

fully susceptible, neither the CSG nor FST would consistently prevent harmful exposure to primaquine. This problem will require clinical studies that would carefully assess the dangers imposed by this vulnerability. The most severe G6PD deficiency variants appear to be most common where P. vivax occurs in greatest abundance, in South and Southeast Asia. 32 Some evidence suggests that P. vivax drives selection for G6PD deficiency, 33 which would require affecting the reticulocytes strictly preferred by this species—natural G6PD activity decays from the highest level in reticulocytes as RBCs age. Populations most likely to benefit from primaquine therapy against relapse may also be at greatest risk of suffering serious harm caused by it.

Le cheminement de ses manuscrits était un thème de prédilection d

Le cheminement de ses manuscrits était un thème de prédilection de nos conversations : l’ont-ils lu ? Le liront-ils ? Qu’en penseront-ils ? Répondront-ils… Cette quête de l’éditeur donnait jusqu’à l’infini à Michel l’opportunité de développer l’une de ses plus belles qualités : la persévérance. Et si c’est à l’œuvre qu’on reconnaît l’artisan, Michel exprimait dans chacune de ses activités le goût du travail bien fait.

Lorsque nous nous étions lancés dans l’écriture d’un atlas de capillaroscopie au début des années 1980, Michel avait décidé d’expliquer chaque image de l’atlas, par un schéma, dessinant les contours à l’encre de chine de chaque capillaire. Il augmentait d’autant le nombre de pages de l’ouvrage sous le regard effrayé de l’éditeur qui nous avait suivis dans cette INCB024360 aventure ! Ses qualités d’écriture et d’analyse, Michel les avaient mises au service du Journal des Maladies Vasculaires. Il était élu à l’unanimité rédacteur en chef le 13 juin 1990, succédant

MK-2206 solubility dmso au Pr Claude Olivier. Pendant plus de 20 ans, Michel assurera cette fonction avec une politique simple : promouvoir la qualité, l’innovation, l’enseignement de la pathologie vasculaire et la défense de la médecine vasculaire. Michel était assisté d’une secrétaire de rédaction sans laquelle je ne suis pas certain qu’il eut accepté de poursuivre cette mission, la très discrète Françoise Staub. Aujourd’hui, Organe du Collège français de pathologie vasculaire Phosphoglycerate kinase et d’autres sociétés, publié par un éditeur prestigieux Elsevier Masson, le Journal des Maladies Vasculaires est un journal en bonne santé dans un monde ou l’édition papier souvent vacille.

Cette bonne santé, on la doit à l’exigence constante de Michel Vayssairat. N’écrivait-il pas lors de sa prise de fonction en 1991 « le nouveau rédacteur en chef porte depuis peu des lunettes mais on ne lui fait pas encore prendre des vessies pour des lanternes ». Michel disait aussi joliment « le Journal des Maladies Vasculaires est au Collège ce que la voile est à la goélette : ils sont indissociables pour le meilleur et pour le pire ». Il était donc logique que, devenant par la même le cinquième président du Collège français de pathologie vasculaire, Michel Vayssairat succède en 2002 à Jean-Daniel Picard qui lui remettait les clés de la maison de l’angiologie. Pendant dix ans, c’est le meilleur qu’il advint. Michel consacrait toute son énergie à défendre l’idéal du Collège, celui d’une société savante accueillante, originale puisque regroupant toutes les disciplines qui touchent à la pathologie vasculaire simplement parce que pour traiter les maladies vasculaires, toutes sont utiles.

While the coming CFP does not arrange for RBM in a systematic and

While the coming CFP does not arrange for RBM in a systematic and formalized sense,

it nevertheless comprises some openings for operators to pursue RBM like arrangements in cooperation with member states, mainly as concerns the implementation of management plans and landing obligations. This work is an outcome selleck inhibitor of the EcoFishMan project (www.ecofishman.com)—a 7th Framework research project that seeks to develop a results based fisheries management alternative in Europe (KBBE; grant agreement nr. FP7-265401). The authors are indebted to project colleagues, stakeholders and external advisors. They are particular grateful to Mogens Schou (affiliated with Danish CQM initiatives), Daryl Sykes (director of the New Zealand Rock Lobster Industry Council), Pamela Maze, Rosemary Hurst and other IPI-145 ic50 experts in New Zealand, who generously offered insights in fisheries management processes in New Zealand and in cases where commercial stakeholder originations have a strong role in management and research. “
“The distribution of many tropical parasitic diseases is a complex interplay of parasite biology (as well as associated vectors

or intermediate hosts thereof), suitability of the surrounding local environment and human-related factors, such as our biology and physiology, demography, and behaviour.1 and 2 Where this complex interplay is permissive it gives rise to a disease-endemic landscape, and where it is not delineates its boundaries or absence. Such patterns can be temporal and operate at different scales, from the macro to the micro, the causal factors for which may or may not transfer Rho across scales.2, 3 and 4 For example, at the macro level, areas may simply be too hot or cold to sustain parasite transmission

and whilst these thermal boundaries may still apply at the micro level, others become more influential, such as the numbers of infected people needed to sustain sufficient parasites in local transmission.5 Thus, at this fine scale level, parasites must exceed certain population thresholds to pass successfully from humans to their vectors/intermediate hosts, and vice versa, or sufficiently contaminate the environment as in the case of soil-transmitted helminths, to safeguard their infection potential(s).6 and 7 Assessing the transmission potential or actual patterns of endemicity at the micro-level is particularly challenging as a variety of potentially unique place-specific factors are involved; foremost, a detailed cartographical knowledge of the local area is needed which can be logistically challenging to record, especially if this knowledge is held verbally alone, i.e. distribution of households within a village.


Moreover, Small molecule library to determine the activity of ACE in TGR(Tie2B1) rats, on the conversion of AngI to AngII, contractile responses induced by AngI pre-incubated for 30 min with lisinopril were tested. Concentration–response curves were obtained incubating non-cumulative concentrations of AngI to avoid desensitization. In the presence of ACE inhibitor there was similar inhibition of the responses throughout all tested concentrations

of the agonist in both strains of the rats (WT, 5C and TGR(Tie2B1), 5D). The pD2 values expressing the potency and the maximal response (Emax) values are presented in Table 1. The ACE activity was also determined using a selective fluorescence substrate assay for ACE with Abz-FRK(Dnp)P-OH as substrate. These results showed that the hydrolysis of the substrate was not different between WT and transgenic rat overexpressing the B1R (Fig. 6). It was found that the cleavage of this substrate was completely abolished by 0.5 μM lisinopril. The expression levels of B2R were determined by real time PCR relative quantification, since the maximum effect induced by

BK in the transgenic TGR(Tie2B1) rats was higher than in the WT rats. Furthermore, expression level of ACE was evaluated. Fig. 7 shows the results about the levels of their expression, which was calculated by fold-up change of the transgenic rat over the control group. The expression level Raf activation of B2R increased about three folds in the TGR(Tie2B1) rat whereas that of ACE mRNA expression

was not significantly different from the control WT rats. Responsiveness of the thoracic aortic rings to angiotensin II (AngII) induced contractile response was assessed to evaluate any cross-talking between kinin and AT1 receptors under conditions where the expression level of B2R was shown to be increased in TGR(Tie2B1) rat. The concentration-responses curves were obtained using non-cumulative manner for stimulations to avoid desensitization. The data show that the vascular reactivity to AngII (Fig. 8) in the aortic rings from TGR(Tie2B1) rats was not altered when compared to that of WT rat. The maximal response click here values (%) were 31 ± 4 (4) for WT and 30 ± 2 (5) for TGR(Tie2B1) and the pD2 values were 7.8 ± 0.2 (4) for WT and 7.9 ± 0.2 (5) for TGR(Tie2B1). In addition, the determination of AT1 receptor mRNA expression revealed that in aorta overexpressing the B1 and B2 receptors, there was no significant difference from the control WT rats (Fig. 7). The present study showed that the vascular reactivity to BK as well as the expression level of B2R mRNA were increased in rats overexpressing the kinin B1R (TGR(Tie2B1)) exclusively in the endothelium. The relaxation of aortic rings induced by BK was significantly greater in this transgenic rat than the control, which was completely abolished by B2R antagonist HOE-140.

2); BGN (Bgn, Gene ID: 12111) (forward 5′-TAGGAAAGATGGATAGACCACAC

2); BGN (Bgn, Gene ID: 12111) (forward 5′-TAGGAAAGATGGATAGACCACAC-3′; reverse 5′-GAACTTGTTGAAGAGAGAACACC-3′; amplicon with 145-bp, GenBank NM_007542.4). The reaction AT13387 datasheet solution was carried out in 96-well plates with a final volume of 20 μL, containing 1 μL of cDNA, 1 μL of probe or set of primers (5 pmol), 10 μL of Jump Start SYBR Green Taq Ready Mix and 8 μL of Nuclease-Free water. The SYBR Green amplification conditions consisted in a initial denaturation of 5 min at 95 °C, followed by 40 cycles of 15 s at 95 °C (denaturation), 30 s at 54 °C (COL1); 59 °C (MMP-2; BIGL); 60 °C (ALP); 60 °C (DSPP) (annealing temperature),

and 30 s at 72 °C (extension). The threshold was set above the non-template control background and within the linear phase of target gene amplification to calculate the cycle number at which the transcript was detected, denoted Cp (Crossing point). Target genes expression were normalized by the reference housekeeping gene glyceraldehyde-3-phosphate dehydrogenase (GAPDH) (Gapdh, Gene ID: 14433) (forward 5′-GTGCTGAGTATGTCGTGGAGT-3′; reverse 5′-TTGTCATATTTCTCGTGGTTCA-3′; amplicon 154-pb, GenBank NM_008084.2) and the mean value for the Control group was

set to 100% of mRNA expression and served as a reference. To evaluate whether PTH administration affect the MMP-2 secretion, MDPC-23 cells were cultured as previously describe in 96-well plate (n = 4). At the end experimental period (3 cycles × 48 h), the cells were washed with PBS and cultured in the absence of FBS for 24 h cAMP at 37 °C in an atmosphere of high humidity and 5% Selleck ZVADFMK CO2 for MMPs secretion. Then, cell culture medium (DMEM) containing the secreted MMPs was collected and frozen at −70 °C. After thawing the protein concentration was determined by a Bio-Rad Protein Assay (Bio-Rad Laboratories, Hercules, CA, USA), using the Bradford method. Fifteen nanograms of the each sample was mixed with non-reducing sample buffer (2% SDS; 125 mM Tris–HCl, pH 6.8, 10% glycerol, and 0.001% bromophenol blue) and resolved in 10% sodium dodecyl sulphate-polyacrylamide gels copolymerized with 1.6 mg/mL of gelatin (Sigma–Aldrich, St. Louis, MO, USA) as substrate. Protein

renaturation was done by incubation of the gels in 2% Triton X-100 (Sigma–Aldrich, St. Louis, MO, USA), and then the gels were immersed in activation buffer (50 mM Tris–HCl, pH 7.4, 5 mM CaCl2) for 16 h at 37 °C. Gelatinolytic activity was detected after staining with Coomassie Brilliant Blue R250 (Bio-Rad Laboratories, Hercules, CA, USA). To confirm that the bands were related to MMP-2 activity, a molecular weight was used and also control reaction was made to inhibit the gelatinolytic activity by adding 2 mM of 1.10-phenanthroline (Sigma–Aldrich, St. Louis, MO, USA), a nonselective zinc chelator, to the activation buffer, confirming the specificity of the reactions. The gel image was obtained by Gel Logic 212 PRO (Carestream Health, Inc., USA) using a Molecular Image Software 5.

Understanding the molecular mechanisms regulating chromosome

Understanding the molecular mechanisms regulating chromosome Gefitinib chemical structure architecture will thus be crucial in future research in this field. A general rule emerges from 3C-based approaches: topological domains associated to open chromatin establish long range contacts with other active domains, whereas repressed chromatin regions tend to cluster together (Figure 2) [18, 22 and 23]. In particular, this has been well documented for H3K27me3 associated

chromatin. For example, FISH studies show that the Drosophila Antp and Abd-B genes, which are separated by 10 Mb and located in the ANT-C and BX-C Hox clusters, co-localize inside a PC focus when repressed, but not when any of them is active. 4C analysis confirms this contact and shows that the BX-C locus can establish several other interactions, mainly with other H3K27me3 genomic domains located on the same chromosome [ 12•]. Importantly, long-range interactions have been reported for transgenes containing regulatory regions of the BX-C including PREs associated with insulator activity, such as Fab7 and Mcp [ 43 and 44], whereas another PRE devoid of insulators,

bxd, does not induce long-range contacts. In keeping with these data, the insulator FG4592 portion of the Mcp and Fab7 are required and sufficient to establish long-range interactions [ 45 and 46], suggesting that PcG proteins may stabilize long-range interactions rather than induce them. On the other side of the coin, contacts can also occur when both target genes are active. Those contacts are functionally regulated because they rely on Trithorax, enhancer specificity and CTCF proteins [ 12• and 46]. These Succinyl-CoA studies thus confirm the segregation between active open chromatin and repressed compact chromatin, because a high frequency of interactions is never observed between active and silenced genes. The same theme emerges from several recent studies that analyzed long-range interactions

in pluripotent stem cells and found significant co-localization of chromatin regions characterized by high pluripotency factor occupancy in mammals [47•, 48•, 49•, 50•, 51• and 52•]. Once again, long-range contacts involved either active genes or silent chromatin, where many long-range interactions involve domains enriched in Polycomb/H3K27me3 in embryonic stem cells. Importantly, loss of the protein Polycomb Eed decreases contacts between Polycomb-regulated regions without altering the overall chromosome conformation [52•]. Long-range interaction of H3K27me3 chromatin domains has also been reported during vernalization in Arabidopsis, when cold induces silencing of the flowering locus c (FLC). Live cell imaging shows that FLC alleles, tagged with the Lac operator system, cluster during cold.

In an experimental study, this significant reduction in the gluco

In an experimental study, this significant reduction in the glucose levels was also confirmed.16 and 38 Contrariwise, Kim et al. observed not in type 1 diabetes significant alteration in glucose levels after administration of MK0431.17 These results show that the potential relation of incretins or incretin mimetics and the type 1 diabetes remain unclear. Anyway, selleck compound Gutniak et al. and Creutzfeldt et al. provide evidence to support the potential utility of incretin-based therapies in the treatment of diabetes mellitus.38, 39 and 40 Lastly, our data also permit to conclude that the animals presented an effective diabetic condition

and the therapy with MK0431 played an important role in the reduction of hyperglycemia condition. The relation existing between salivary glands and pancreas has been described in literature. selleck kinase inhibitor Some authors also demonstrated that these organs may share a common antigen that might be the target of the autoimmune process in the type 1 diabetes.41 Similarly, in the present study, the salivary glands of diabetic animals were target

of this hyperglycaemic condition, presenting structural changes, characterized by pleomorphic acini, minor spatial area occupied by secretory epithelium and a higher volume density of collagen fibres. In contrast, recovery of the glandular structure was observed in the group treated with MK0431. The submandibular glands of treated animals presented a higher recovery, characterized by a minor quantity of collagen fibres and organization of secretory epithelial cells. This positive finding might be explained by physiological and anatomical similarity between the submandibular gland and pancreas,42, 43 and 44 thus responding better to the treatment with MK0431. The morphological characteristics of salivary glands in healthy animals, the relationship between these normal tissues and incretins, and the effects of diabetes on these organs have been documented.7, 45 and 46 Simões et al. observed the accumulation of lipid droplets in the glands of hyperglycaemic rats, elements characteristic in

processes of tissue damage.47 Also, alterations in saliva components were observed in salivary Amino acid glands of diabetic animals and the tissue responses to this condition were different when compared to the mucous and serous glands.48 and 49 Additionally, the effects of diabetes have also been described in salivary glands of humans, characterized by small acini, a bigger number of lipid intracytoplasmic droplets in the acinar and ductal cells, increased volumes of fibrous tissue, as well as an abundant adipose infiltration in the stroma.41, 50 and 51 To reverse these damages, treatments with incretins and incretin mimetics can be an important tool in recovering of tissues. However, despite of promising results, the MK0431 can be related also to cellular complications and doubts still exist regarding the total efficacy of this treatment in different cases.

Spherical nanoparticles may be found in stabilised colloidal SAS

Spherical nanoparticles may be found in stabilised colloidal SAS suspensions. SAS, including colloidal and surface-treated forms, have widely been used in topical and

oral medicines, food and cosmetics for decades without evidence of adverse human health effects. Standard ecotoxicity and toxicity tests generally demonstrated the biological inertness of SAS, and SAS were considered safe if occupational standards and use recommendations are followed (Becker et al., 2009, ECETOC, 2006, IARC, 1997, Lewinson et al., 1994 and OECD, 2004). Nevertheless a discussion about hazards and risks of “nanosilica” has recently started calling into question the safety of mTOR inhibition SAS materials which are made up of primary particles in the nano-size range (Napierska et al., 2010 and Dekkers et al., 2010). This discussion has prompted this work to investigate whether the mode of action (MOA) or mechanisms of toxicity of so-called “nano-SAS” or “nanosilica” are different from those of the commercial SAS forms. To this end a systematic literature search was undertaken to identify relevant publications. The studies considered in this review were selected according to commonly accepted criteria of relevance, adequacy, reliability and validity (Klimisch et al., 1997 and OECD, 2005). In addition, studies with critical results and

those not yet covered in available authoritative reviews (IARC, 1997 and OECD, 2004) were included. There are three main types of silica (silicon dioxide), which are all found under CAS No. 7631-86-9, i.e., (1) crystalline silica, Gemcitabine order (2) amorphous silica (naturally occurring or as a by-product in the form of fused silica or silica fume), and (3) synthetic amorphous silica (SAS), including silica gel, precipitated silica, pyrogenic (fumed) silica and colloidal silica (silica sol). Only the manufactured forms of amorphous silica (SAS) will be dealt with in the following article, i.e., SAS produced by a wet process and described by CAS number 112926-00-8 (includes silica gel, precipitated silica and colloidal silica) and SAS produced by a thermal process described by CAS number 112945-52-5 (pyrogenic

silica). It also includes the surface-treated, hydrophobic SAS types, i.e., silica dimethicone silylate, silica dimethyl silylate and silica silylate (CAS 67762-90-7, 68611-44-9 and 68909-20-6). In general, SAS contains no detectable amounts of crystalline Mannose-binding protein-associated serine protease silica (detection limits vary between 0.01 and 0.3% by weight, depending on the method used; ECETOC, 2006, pp. 12–14). SAS also contains fewer impurities than biogenic amorphous silica which is obtained from various sources such as the shell wall of phytoplankton or the epidermis of vegetables, or non-biogenic vitreous amorphous silica. SAS can be distinguished from other forms of amorphous silica by its high chemical purity, the finely particulate nature and by characteristics of the particles observable by electron microscopy, e.g., shape, structure, and degree of fusion ( Fig. 1).