In contrast, when complemented only with panC (strain ReTV1-5) no growth occurred in the absence of pantothenate. These results strongly suggest that the panCB genes form a single transcriptional unit. As see more expected, wild type growth of panB mutant ReTV2 was recovered by complementation with the panCB genes or with the panB gene (strains ReTV2-4 and ReTV2-6 respectively). The occurrence of panCB genes in selleck inhibitor plasmids is highly conserved among R. etli and R. leguminosarum strains but not in other members of the Rhizobiales with multipartite genomes To investigate whether the presence of the panCB genes in plasmids is a common characteristic of the Rhizobiales, we examined the location of

panCB genes in 22 members of the Rhizobiales having fully sequenced multipartite genomes (Table 2). To date, the genomes of seven R. etli strains, in addition to CFN42, have been totally sequenced [15]. However, with the exception of strain CIAT 652, the genomes were released as draft assemblies, precluding panCB localization. We experimentally determined the localization of panCB

genes in the genome of four of these R. etli strains (CIAT 894, Kim5, 8C-3, and IE4771) by hybridization of their plasmid profiles with [32P]dCTP-labelled panC and panB genes from CFN42 under high stringency conditions. Both probes produced intense hybridization signals on the same plasmid of each strain, indicating that the panCB genes are also plasmid-borne in these R. etli strains (Table 2). Coincidentally, in the three R. leguminosarum strains

with fully sequenced genomes reported in the NCBI click here through database, the panCB genes are assigned to plasmids. In contrast, in other species of Rhizobiales with multipartite genomes, the panCB genes are always confined to the chromosome, or to chromosome I in those species harboring two chromosomes, with exception of Agrobacterium tumefaciens C58 which carries panCB on the linear chromosome II and Methylobacterium nodulans ORS2060 that carries panC on their single chromosome and panB on plasmid pMNOD02 (Table 2). Table 2 Localization of the panCB genes in representative members of the Rhizobiales with multipartite genomes. Strain     Localization of   Genome number Chr Structure of Plasmids panC panB Brucella abortus bv. 1 str. 9-941 2 0 ChrI ChrI B. melitensis 16M 2 0 ChrI ChrI B. ovis ATCC 25840 2 0 ChrI ChrI Sinorhizobium meliloti 1021 1 2 Chr Chr S. medicae WSM419 1 3 Chr Chr Ochrobactrum anthropi ATCC 49188 2 4 ChrI ChrI Agrobacterium radiobacter K84 2 3 ChrI ChrI A. vitis S4 2 5 ChrI ChrI A. tumefaciens C58 2 2 ChrII ChrII Rhizobium etli CFN42 1 6 p42f p42f R. etli CIAT 652 1 3 pc pc R. etli CIAT 894* 1 4 pd pd R. etli Kim5* 1 4 pc†/pd† pc†/pd† R. etli IE4771* 1 4 pd pd R. etli 8C-3* 1 3 pc pc R. leguminosarum bv. viciae 3841 1 6 pRL12 pRL12 R. leguminosarum WSM1325 1 5 pR132501 pR132501 R. leguminosarum WSM2304 1 4 pRLG201 pRLG201 Rhizobium sp.

Nature 2011,473(7346):174–180.PubMedCrossRef this website 3. Wu GD, Chen J, Hoffmann C, Bittinger K, Chen YY, Keilbaugh SA, Bewtra M, Knights D, Walters WA, Knight R, Sinha R, Gilroy E, Gupta K, Baldassano R, Nessel L, Li H, Bushman FD, Lewis JD: Linking Long-Term Dietary Patterns with Gut Microbial Enterotypes. Science 2011,334(6052):105–108.PubMedCrossRef 4. Turnbaugh PJ, Hamady M, Yatsunenko T, Cantarel BL, Duncan A, Ley RE,

Sogin ML, Jones WJ, Roe BA, Affourtit JP, Egholm M, Henrissat B, Heath AC, Knight R, Gordon JI: A core gut microbiome in obese and lean twins. Nature 2009,457(7228):480–484.PubMedCrossRef 5. Turnbaugh PJ, Ley RE, Hamady M, Fraser-Liggett CM, Knight R, Gordon JI: The human microbiome project. Nature 2007,449(7164):804–810.PubMedCrossRef 6. Freitas M, Tavan E, Cayuela

C, Diop L, Sapin C, Trugnan G: Host-pathogens cross-talk. Indigenous bacteria and probiotics also play the game. Biol Cell 2003,95(8):503–506.PubMedCrossRef 7. Shirazi T, Longman RJ, Corfield AP, Probert CS: Mucins and inflammatory bowel disease. Postgrad Med J 2000,76(898):473–478.PubMedCrossRef

buy NU7026 8. Wacklin P, Makivuokko H, Alakulppi N, Nikkila J, Tenkanen H, Rabina J, Partanen J, Aranko K, Matto J: Secretor genotype (FUT2 gene) is strongly associated with the composition of Bifidobacteria in the human intestine. PLoS One 2011,6(5):e20113.PubMedCrossRef 9. Hoskins LC, Boulding ET: Degradation of blood group antigens in human colon ecosystems. I. In vitro production of ABH blood group-degrading enzymes by enteric bacteria. J Clin Invest 1976,57(1):63–73.PubMedCrossRef 10. Moulds JM, Nowicki S, Moulds JJ, Nowicki BJ: Human blood groups: incidental receptors for JQ-EZ-05 ic50 viruses and oxyclozanide bacteria. Transfusion 1996,36(4):362–374.PubMedCrossRef 11. Boren T, Falk P, Roth KA, Larson G, Normark S: Attachment of Helicobacter pylori to human gastric epithelium mediated by blood group antigens. Science 1993,262(5141):1892–1895.PubMedCrossRef 12. Uchida H, Kinoshita H, Kawai Y, Kitazawa H, Miura K, Shiiba K, Horii A, Kimura K, Taketomo N, Oda M, Yajima T, Saito T: Lactobacilli binding human A-antigen expressed in intestinal mucosa. Res Microbiol 2006,157(7):659–665.PubMedCrossRef 13.

In more convenient units, ϵ g and , the expression of energy (10) can be written in a simpler form suitable for graphical representations: (11) where . For comparison (see (10)), in the case of a parabolic dispersion law (e.g., for QD consisting of GaAs), the total energy Bafilomycin A1 price in the strong SQ is given as [28]: (12) Weak size quantization regime In this regime, when the condition R 0 ≫ a p takes place, the system’s energy is caused mainly by the electron-positron Coulomb interaction.

In other words, we consider the motion of a Ps as a whole in a QD. In the case of the presence of Coulomb interaction between an electron and positron, the Klein-Gordon equation can be written as [41]: (13) where e is the elementary Combretastatin A4 molecular weight charge. After simple transformations, as in the case of a strong SQ regime, the Klein-Gordon equation reduces to the Schrödinger equation with a certain

effective energy, and then the wave function of the system can be represented as: (14) where . Here, describes the relative motion of the electron and positron, while describes the motion of the Ps center of gravity. After switching to the new coordinates, the Schrödinger equation takes the following form: (15) where is the mass of a Ps. One can derive the equation for a Ps center of gravity, 4-Aminobutyrate aminotransferase after www.selleckchem.com/products/mrt67307.html separation of

variables, in the and a p units: (16) or (17) where ϵ R is the energy of a Ps center of gravity quantized motion and L is the orbital quantum number of a Ps motion as a whole. For energy and wave functions of the electron-positron pair center of gravity motion, one can obtain, respectively, the following expressions: (18) (19) where N and M are, respectively, the principal and magnetic quantum numbers of a Ps motion as a whole. Further, let us consider the relative motion of the electron-positron pair. The wave function of the problem is sought in the form . After simple transformations, the radial part of the reduced Schrödinger equation can be written as: (20) where the following notations are introduced: . The change of variable transforms Equation 20 to: (21) where the parameter is introduced. When ξ → 0, the desired solution of (21) is sought in the form χ(ξ → 0) = χ 0 ~ ξ λ [45, 46]. Substituting this in Equation 21, one gets a quadratic equation with two solutions: (22) The solution satisfying the finiteness condition of the wave function is given as . When ξ → ∞, Equation 21 takes the form . The solution satisfying the standard conditions can be written as [45].

125 – 0.25 0.25 – 0.5 0.064 – 0.125 CTX-M-15+ CIT (n = 1) 120 min and 24 h *peaks m/z: 476.5, 498.5, 520.5 and 542.5 Da. A synthesis of the results showing the species, resistance mechanism and MIC range in the test panel and validation panel in relation to the results in the hydrolysis assay based on ertapenem. Pseudomonas aeruginosa (n = 25) Six out of elevenVIM producing P. aeruginosa, as well as the IMP-14-producing isolate tested, hydrolysed ertapenem after 120 minutes of incubation with the specific ertapenem hydrolysis peak pattern. The hydrolysis was fully inhibited in the presence of DPA in all cases. Ertapenem was not hydrolysed by the non-carbapenemase producing (no carbapenemase

confirmed genetically find more or phenotypically), carbapenem resistant, P. aeruginosa isolates (n = 10). Of the 4 P. aeruginosa isolates included in the validation panel (three VIM-1 and one

VIM-2) were correctly assigned as carbapenemase producers (both VIM-1). The carbapenemase production was inhibited Angiogenesis inhibitor by DPA both for VIM and IMP positive strains. Prolonged incubation (24 h) did not reveal any signs of hydrolysis in the strains tested negative after 120 min incubation (one VIM-1 and one VIM-2). There was no linkage between VIM-type and hydrolysis results. A summary of the results is presented in Table 1. Other species (Acinetobacter baumannii (n = 4), Escherichia coli (n = 3) None of the 4 Acinetobacter baumannii group isolates(OXA-23 like (n = 2), OXA-24-like (n = 1) and OXA-58 like (n = 1)) included in the validation panel hydrolysed ertapenem within 120 min incubation. All Teicoplanin isolates, however, displayed the specific pattern of ertapenem hydrolysis after a prolonged incubation (24 h). The two isolates of E. coli only producing a classical selleck compound ESBL-enzyme (two CTX-M-1 group and one CTX-M-1 group plus CIT-group plasmid mediated AmpC) did not hydrolyse ertapenem at any time point. The OXA-48 positive isolate of E. coli did not hydrolyse ertapenem

within 2 h, but prolonged incubation (24 h) revealed hydrolysis. A summary of the results is presented in Table 1. Discussion The drastic increase of isolates with the ability to produce carbapenemases in Enterobacteriacae, Acinetobacter spp. and P. aeruginosa rapidly challenges the treatment concept of severely ill patients [1]. Whether the carbapenem resistance is due to carbapenemase production or other mechanisms is considered important for infection control teams. Molecular methods are available for the verification of the genes responsible for carbapenemase production but have the limitation of not detecting new mechanisms [9–11]. The phenotypic assays so far on the market have problems with the time to result, isolates with low expression of the carbapenemase genes and that specific inhibitors are not available for several enzymes [2].

Therefore, Livin as a target gene for treating bladder cancer has a good application prospect. Antisense nucleic acid is a naturally existing or synthetic nucleotide sequence. Livin ASODN hybridizes with target genes through Watson Crick principle of complementary base pairing to prevent gene expression, inhibit cell proliferation, promote apoptosis, and achieve the purpose of preventing or treating tumors. The natural oligonucleotide

learn more is easily degraded, but Crenolanib research buy phosphorathioate modifying can increase the capacity of its tolerance to nucleic acid hydrolysis, with good solubility and hybridization properties. The effectiveness and safety have been universally accepted by researchers. Currently the antisense oligonucleotide with bcl-2 as the target gene (trade name: Oblimersen) is in Phase III clinical trials with the permit of FDA (mainly treat malignant melanoma, chronic lymphocytic leukemia, multiple myeloma, etc.) [19]. The drug achieves the purpose of cancer treatment by inhibiting the expression of bcl-2 inside the tumor cells and inducing the tumor cell apoptosis. There are also a variety of antisense

oligonucleotides anticancer drugs in clinical trials [20, 21]. In the present study, phosphorathioate modifying greatly enhanced the anti-ribozyme decomposition capacity of www.selleckchem.com/products/PF-2341066.html Livin ASODN. The supplement of cationic liposome transfection further increased its stability and improved the ability of uptake by cells. Using RT-PCR, Western blot, immunocytochemistry, immunohistochemistry, we found that Livin ASODN could inhibit the expression of Livin mRNA and protein. We further observed that the cell growth was inhibited and the apoptosis increased from MTT, flow cytometry, TUNEL method and morphological observations. almost Caspases protein plays an important role in apoptosis. Most of the stimuli induce apoptosis through the Caspase protein cascade activation reactions. Caspases protein family has more than 10 members. Literatures have reported that Livin can interact with Caspase-3, -6, -7, -8, -9, -10 [22] (especially Caspase 3) to inhibit the process of apoptosis. Using

immunohistochemistry, we observed that after the injection of Livin ASODN, the expression of Caspase 3 in tumor tissues increased, which was probably because Livin ASODN inhibited the expression of Livin and then removed the binding inhibition to Caspase 3. Besides, Caspase 3 removal function also enhanced, which lead to increased cell apoptosis. In conclusion, Livin ASODN could specifically inhibit the expression of Livin in human bladder cancer cell 5637 and induce apoptosis of bladder cancer cells. It may be a potential and most promising strategy for bladder cancer. Acknowledgements This study was supported by research grant from Research Development Foundation of Health Bureau of ChongQing (No. 04-2-131). References 1.

After each tissue type removal, i.e., tumoral and normal epithelium and stromal tissue (avoiding capturing endothelial and immune cells), total RNA was extracted, amplified and hybridized onto Affymetrix GeneChip

U133 X3P arrays. Genes differentially expressed between groups were identified using Limma algorithm (p < 0.01) of the Bioconductor software suite and further assessed using gene ontology analysis, performed using the GO Tree Machine tool. When compared to epithelial tumoral cells, stromal cells presented enriched categories related to “T cell receptor signaling pathway” (p = 0.004); “protein folding” (p = 0.008); and “chemotaxis” (p = 0.006). The most prominently enriched category

JNK animal study in tumoral versus normal breast epithelium were “inflammatory response” (p = 0.002) and “response to stress” (p = 0.009). The evaluation of components separately resulted in distinct signatures that should help to better understand some of the OSI-906 clinical trial molecular mechanisms involved in the complex heterotypic signaling between epithelial cells and fibroblasts. Supported by FAPESP/CNPq. Poster No. 32 HIF2alpha Overexpression Drastically Reduces HIF1alpha Protein Amounts in Melanoma Cells under Hypoxia Anne-Lise Steunou 1 , Laurence Nieto1, Eric Clottes1 1 Department of “Biologie du Cancer”, Institut de Pharmacologie et de Biologie Structurale-UMR 5089, Toulouse, France Hypoxia inducible transcription factors (HIF) are

key regulators of cellular adaptation to hypoxia in normal FK228 chemical structure but also in pathologic conditions such as cancer development. They are involved in melanocyte transformation, tumour progression and metastasis of melanoma cells. HIF is a heterodimeric protein composed of an alpha subunit regulated by oxygen pressure and a beta subunit constitutively expressed. In melanoma, HIF1a and HIF2a subunits are recovered. Although both HIFa subunits are structurally homologous, they see more exhibit different roles sometimes antagonist in the tumoral development. In order to understand these different behaviours, stable human melanoma cell lines overexpressing HIF2a protein were constructed. Surprisingly, in these cells, a decrease in HIF1a protein expression was monitored under hypoxia. HIF1a protein underexpression was inversely correlated with HIF2a protein amount. To explain this observation, transcript concentrations of HIF1a and aHIF were measured using a qRT-PCR assay. aHIF is a natural antisense of HIF1a transcript complementary to HIF1a mRNA 3′untranslated region, suspected to negatively regulate HIF1a mRNA amounts. Under hypoxia, aHIF RNA quantity was strongly increased in control transfected melanoma cells (empty vector) whereas aHIF induction was totally lost in stable cell lines overexpressing HIF2a.

We can thus re-interpret the higher robustness found for Amazonia: it suggests a high proportion of more uniformly distributed species with medium and larger numbers of species occurrences, and a low proportion of small-clustered species and species with few occurrences. The LOOCV approach does not account for errors due

to heterogeneous data quality or sampling effort. Whereas we integrated a strategy to adjust for heterogeneous spatial sampling effort at the level of species richness, we did not include an adjustment for the fact that more https://www.selleckchem.com/products/tariquidar.html recent monographs will be more complete in terms of both taxa and occurrences considered. For the future, the interpolation process could be altered to include an additional weighting at species level. Furthermore, our maps will improve if more data based on future monographs were to be included in the analysis. The results identified here are not absolute estimates of species richness per quadrat. To obtain a rough estimate of the absolute figures, the numbers per quadrat found need to be multiplied by the factor 20, since our data set represents approximately

about 5% of the angiosperm flora occurring in the Neotropics. Following this estimation, our uppermost results would lie in close proximity to the uppermost results of Barthlott et al. (2005) suggesting more than 5,000 vascular plant species in the most species-rich 10,000 km2 units, and Selleckchem AZD6738 that of Kreft and Jetz (2007), modeling 6,500 species at maximum per most species-rich 1° quadrats. Hydroxychloroquine cost Although our species richness map can only approximate ‘real patterns’, this consistency broadly supports our

estimation of distribution patterns. Narrow endemic species Compared with BMS202 clinical trial previous work (Morawetz and Raedig 2007), in spite of considering more species, a similar number of species is identified as narrow endemic species. Previously, all species occurring in three or fewer quadrats were defined as narrow endemic species irrespective of distance between species occurrences, while in the present work only those species that occurred in five or less quadrats after interpolation with the maximum distance of five quadrats qualified as narrow endemic. Although the threshold of five quadrats appears more generous, the method is more rigorous in that it considers spatial distance. The main differences seen between Morawetz and Raedig (2007) and the present study are the absences of some species in southeastern Amazonia and in the Cerrado and Caatinga (two Brazilian floristic provinces) whose recorded occurrences were too geographically distant to be considered narrow endemic. The analysis of narrow endemic species revealed two shortcomings of our interpolation method: first, if quadrats hold no species after interpolation, no adjustment of sampling effort can be applied. Considering the large number of empty quadrats, the map of narrow endemism (Fig. 6a) might reflect sampling effort more than distribution patterns.

Acknowledgements and Funding We thank Franziska Reipsch and Katrin Nerger for excellent technical assistance. The study was supported by funding and supply of FWGE by Biropharma Ltd, Kunfeherto, Hungary. References 1. Telekes A, Hegedus M, Chae CH, Vekey K: Avemar (wheat germ extract) in cancer prevention and treatment. Nutr Cancer 2009, 61:891–899.PubMedCrossRef 2. Johanning GL, Wang-Johanning F: Efficacy of a medical nutriment in the treatment of cancer. Altern Ther Health Med 2007, 13:56–63. quiz 64–55PubMed 3. Illmer C, Madlener S, Horvath Z, Saiko P, Losert A, Herbacek I, Grusch M, Krupitza

G, Fritzer-Szekeres M, Szekeres T: Immunologic and biochemical JQEZ5 mouse effects of the fermented wheat germ extract Avemar. Exp Biol Med (Maywood) 2005, 230:144–149. 4. Fajka-Boja R, Hidvegi M, Shoenfeld Y, Ion G, Demydenko D, Tomoskozi-Farkas R, Vizler C, Telekes A, Resetar A, Monostori E: Fermented wheat germ extract induces apoptosis and downregulation of major histocompatibility complex

class I proteins in tumor T and B cell lines. Int J Oncol 2002, 20:563–570.PubMed 5. Hidvegi M, Raso E, Tomoskozi-Farkas MAPK inhibitor R, Paku S, Lapis K, Szende B: Effect of Avemar and Avemar + vitamin C on tumor growth and metastasis in experimental animals. Anticancer Res 1998, 18:2353–2358.PubMed 6. Boros LG, Nichelatti M, Shoenfeld Y: Fermented wheat germ extract (Avemar) in the treatment of cancer and autoimmune diseases. Ann N Y Acad Sci 2005, 1051:529–542.PubMedCrossRef 7. Comin-Anduix B, Boros LG, Marin S, Boren J, Callol-Massot C, Centelles JJ, Torres JL, Agell N, Bassilian S, selleck inhibitor Cascante M: Fermented wheat germ extract inhibits glycolysis/pentose cycle enzymes and induces apoptosis through poly(ADP-ribose) polymerase activation in Jurkat T-cell leukemia tumor cells. J Biol Chem 2002, 277:46408–46414.PubMedCrossRef 8. Saiko P, Ozsvar-Kozma M, Madlener S, Bernhaus A, Lackner A, Grusch M, Horvath Z, Krupitza G, Jaeger W, Ammer K, Fritzer-Szekeres almost M, Szekeres T: Avemar, a

nontoxic fermented wheat germ extract, induces apoptosis and inhibits ribonucleotide reductase in human HL-60 promyelocytic leukemia cells. Cancer Lett 2007, 250:323–328.PubMedCrossRef 9. Boros LG, Cascante M, Lee WN: Metabolic profiling of cell growth and death in cancer: applications in drug discovery. Drug Discov Today 2002, 7:364–372.PubMedCrossRef 10. Boros LG, Lapis K, Szende B, Tomoskozi-Farkas R, Balogh A, Boren J, Marin S, Cascante M, Hidvegi M: Wheat germ extract decreases glucose uptake and RNA ribose formation but increases fatty acid synthesis in MIA pancreatic adenocarcinoma cells. Pancreas 2001, 23:141–147.PubMedCrossRef 11. Shao J, Zhou B, Chu B, Yen Y: Ribonucleotide reductase inhibitors and future drug design. Curr Cancer Drug Targets 2006, 6:409–431.PubMedCrossRef 12.

In fact, discrepancies and limitations of these markers for Cryptosporidium typing have been reported. Hunter and colleagues [37] described the difficulty in interpreting the presence of different subtypes in outbreak setting and Proteasome activity Widmer [38] reported that gp60 might not be a reliable

marker of C. parvum and C. hominis population structure. The ten novel loci, described in this study, showed excellent discriminatory power and consistency to assess phylogenetic relationships at the species and infra-species levels. These findings suggest that these loci could be alternative valuable genotyping and subtyping targets for Cryptosporidium. RG-7388 price However, their stability should be assessed in an extensive collection of isolates from different subtype families and geographical locations to validate their discriminatory power. Conclusions In this study, comparative genomics were used to identify putative C. parvum and C. hominis species-specific genes. Despite the fact that the majority of the predicted genes were common to both species and some to C. meleagridis, experimental evidence was found for one specific gene for each species. The ten novel genetic loci studied showed an interesting polymorphism. In fact, sequence Cell Cycle inhibitor analysis of PCR products revealed multiple SNPs, the majority

of which were species-specific. These SNPs were stable and consistent across Cryptosporidium species and subtypes. These results showed

that the ten novel genetic loci can potentially be used to assess the phylogenetic distance and relationships at the species and infra-species level of human infective Cryptosporidium isolates. In addition, the paired SNP analysis was found to be a good strategy to assess the genetic divergence of the isolates tested. Methods Reciprocal Blast was used to identify genes with high sequence variability between C. parvum and C. hominis. This is a variant of Blast (Basic local alignment search tool), originally described by Altschul and colleagues [39] and is a common computational tool for predicting putative orthologs http://​www.​ncbi.​nlm.​nih.​gov/​blast/​blast_​overview.​shtml. Subsequently, each of the ~ 3900 genes of C. parvum and C. hominis was assigned a similarity score. Only sequences new which returned genes with less than 10% sequence similarity from the other genome were considered. These coding sequences are putatively species-specific genes. A secondary screen was performed as follows: each gene was individually tested using Blastn algorithm http://​blast.​ncbi.​nlm.​nih.​gov/​Blast.​cgi to confirm specificity and reveal any sequence similarity to genes from other Cryptosporidium species. Furthermore, orthology queries were performed using CryptoDB database. Whenever a gene showed sequence similarity, it was eliminated from the selection. This secondary screen increased the prediction stringency.

F. (2004). Adsorption and thermal condensation mechanisms of amino acids on oxide supports. 1.Glycine on Silica. Langmuir, 20:914–923. Stievano, L., Piao,

L. Y., Lopes, I., Meng, M., Costa, D., and Lambert J. F. (2007). Glycine and lysine adsorption and reactivity on the surface of amorphous silica. European Journal of Mineralogy, 19:321–331 E-mail: irene.​lopes@upmc.​fr Interaction of Amino Acids in Mineral Fludarabine mw Surfaces and Their Relevance in Chemical Evolution L. López-Esquivel Kranksith1, A. Negrón-Mendoza1, G. Cocho-Gil2, S. Ramos-Bernal1 1Instituto de Ciencias Nucleares; 2Instituto de Física Universidad Nacional Autónoma de Mexico (UNAM) Mexico D.F. Laboratory studies have been carried out simulating the chemical evolution stage of the Selleckchem LY3039478 possible conditions on the primitive Earth. Experiments with various solids (silica, clays, and aluminum-silicates) have shown that they could act not only as surfaces of support, but also as catalysts (Ferris and Ertem, 1992). On the other hand, studies of interstellar matter reveal

the presence of complex organic molecules such as polycyclic aromatic hydrocarbons (PAH), fullerenes and carbon nanotubes (CNTs) (Georgakilas, et al. 2000), acetamide (a precursor of amino acids), simple amino acids and sugars. The questions then arise: How these molecules can survival? Which are the mechanisms involved? In an attempt to answer these questions a series of experiments were undertaking with selected Thiazovivin chemical structure compounds and we study the survival of molecules, such as amino acids, in a hostile high radiation field while they are adsorbed environment (Kawasaki, et al., 2006). To this end, we analyzed the adsorption of amino acids in clay mineral, charcoal (PAC) and

carbon nanotubes (CNTs) as possible phases that may ocurred in the primitive Earth or in extraterrestrial environments. We also studied further the behavior of amino acids Reverse transcriptase adsorbed in these solid surfaces, in different conditions of pH, concentration and levels of irradiation, simulating a high radiation field in the early Earth conditions. The analisis of the samples were performed by UV–vis spectroscopy, X-rays and infrared spectroscopy. Trials adsorption with, Aspartic (Asp) and Glutamic (Glu) acids in sodium montmorillonite were conducted for different times of contac. The adsorption for Asp was of 98% and for Glu was of 60%. In the case of Glu, an interest phenomenom took place and interaction with clay generates a visible coloration lemon-yellow in the clay. This may be related to the interactions between cationic links with clay and the molecular structure a this amino acid. It is also important to emphasize that this clay could promote the catalysis of other compounds, using as a precursor Glu. The complex clay-Glu, may form in this condition pyroglutamic acid (2-oxotetrahidropirrol 5-carboxylic acid), a chemical form of internal protection of glutamic acid, which can be obtained relatively easily, from a catalytic dehydration reaction (Yun, et al.