We conclude that CLU could be a potential molecular marker to predict chemoresistance in patients with ovarian cancer. Thus, CLU gene seems to be a key element regulating chemo-response/chemo-resistance to TX. This gene product might be a potential therapeutic target to overcome the resistance to TX and improve the subsequent survival in ovarian cancer patients. Acknowledgements

We thank Dr. Takahiko Kobayashi and Dr. Shoichi Inoue for their technical advices.. We also thank Dr. Martin Gleave for providing OGX-011. This find more study was supported in part by a grant-in-aid HW for Scientific Research (C 22591844) from the Ministry of Education, Culture, Sports, Science and Technology of Japan. References 1. Matsumoto Y, Takano H, Fojo T: Cellular adaptation Sirolimus concentration to drug exposure: evolution of the drug-resistant phenotype. Cancer Res 1997, 57:5086–5092.PubMed 2. Yap TA, Carden CP, Kaye SB: Beyond chemotherapy: targeted therapies in ovarian cancer. Nature Rev Cancer 2009, 9:167–81.CrossRef 3. Jenison EL, Montag AG, Griffiths CT, Welch WR, Lavin PT, Greer J, et al.: Clear cell adenocarcinoma of the ovary: a clinical analysis and comparison with serous carcinoma. Gynecol Oncol 1989, 32:65–71.PubMedCrossRef 4. Goff BA, Sainz de la Cuesta R, Muntz

HG, Fleischhacker D, Ek M, Rice LW, et al.: Clear cell carcinoma of the ovary: a distinct histologic type with poor prognosis and resistance to platinum-based chemotherapy in stage III disease. Gynecol Oncol 1996, 60:412–7.PubMedCrossRef 5. Miller M, Ojima I: Chemistry and Chemical biology of taxan anticancer agents. The Chem Record 2001, 1:195–211.CrossRef 6. Sugiyama T, Kamura T, Kigawa J, Terakawa N, Kikuchi Y, Kita T, et al.: Clinical characteristics of clear cell carcinoma of the ovary: a distinct histologic type with poor prognosis and resistance to platinum-based chemotherapy. Cancer 2000, 88:2584–9.PubMedCrossRef 7. Itamochi H, Kigawa J, Sugiyama T, Kikuchi Y, Suzuki M, Terakawa N: Low proliferation activity may be associated with chemoresistance

in clear cell carcinoma of the ovary. Obstet Gynecol 2002, DOK2 100:281–7.PubMedCrossRef 8. Reed E, Yu JJ, Davies A, Gannon J, Armentrout S: Clear cell tumors have higher mRNA levels of ERCC1 and XPB than other histological types of epithelial ovarian cancer. Clin Cancer Res 2003, 9:5299–305.PubMed 9. Trougakos IP, So A, Jansen B, Gleave ME, Gonos ES: Silencing expression of the clusterin ⁄/apolipoprotein j gene in human cancer cells using small interfering RNA induces spontaneous apoptosis, reduced growth ability, and cell sensitization to genotoxic and oxidative stress. Cancer Res 2004, 64:1834–42.PubMedCrossRef 10. Shannan B, Seifert M, Leskov K, Willis J, Boothman D, Tilgen W, et al.: Challenge and promise: roles for clusterin in pathogenesis, progression and therapy of cancer.

Cells

were then lysed with 0.2% triton-X 100 diluted in water. Finally, serial dilutions of the cell lysate were plated for bacterial counting. CFU of intracellular bacteria were expressed as the average of three independent selleck chemicals llc gentamicin assays performed in triplicate. Invasion rate was calculated as the ratio of CFU counts. Confocal laser scanning Bacteria were stained as described by Lee et al. (2004) [42]. Stationary phase culture of recombinant or wild type L. lactis, were washed twice in PBS and stained with 50 μM of green fluorescent dye carboxyfluorescein succinimidyl ester (CFSE) at 37°C for 20 min under constant shaking in the dark. CFSE labeled bacteria were used to perform the invasion assay as described above in non-differentiated Caco-2 cells grown on filter inserts. After 1 h of infection, cells were washed three times with PBS and fixed using 4% paraformaldehyde. Cell membranes were stained with 1 μM Vybrant® CM-DiI cell-labeling solution (Invitrogen) for 1 h at room temperature. Cells were mounted in Vectashield solution (Vector Labs, Burlingame, USA) to minimize photobleaching. Confocal

images were obtained using a Zeiss LSM 510 system consisting of a Zeiss Axioskop with a Zeiss Plan Neofluar 63x NA 1.3 oil objectives. Stacks of images were reconstructed using Zeiss LSM software. β-Lactoglobulin (BLG) expression by human intestinal epithelial cells after incubation click here with bacteria In order to measure BLG expression and secretion by human epithelial

cells the gentamicin survival assay was performed with Caco-2 cells as described above, however, bacteria and Caco-2 cells were incubated for three hours. After gentamicin treatment, plates were maintained for 72 h at 37°C, in 5% CO2. Supernatant was collected by centrifugation at 78.2 g (800 rpm) for 10 min and stored at -80°C. One mL of PBS supplemented with a cocktail of protease inhibitors (Roche) was then homogenized by sonication (3 times 10 s). Samples were kept at -80°C and used to measure BLG production using an Enzyme ImmunoAssay (EIA) described in the next acetylcholine section. Enzyme immunometric assay (EIA) for quantification of bovine β lactoglobulin in human epithelial cells The method used for BLG quantification is described elsewhere [43]. In summary, 96 microtitre plates were coated with 3.5 μg/ml of anti-BLG monoclonal antibody, diluted in 50 mM phosphate buffer (PB) pH 7.4, and incubated overnight at room temperature. After washing, plates were blocked with EIA buffer (0.1 M PB pH 7.4; 1 g/1 L BSA; 0.15 M NaCl; 0.001 M Na2EDTA; 0.1 g/1 L sodium azide) and stored sealed at 4°C until use. Standard (recombinant BLG) and samples diluted in EIA buffer were added and kept at 4°C for 18 h. After this time, plates were extensively washed and then acetylcholinesterase conjugated monoclonal anti-BLG antibody (1 Ellman Unit/ml) was added for 18 h at 4°C.

In poultry production, the whole flock is generally treated by adding this compound to the drinking water, whereas, in cattle or pig production, treatment is often restricted to diseased animals. As a result, the highest levels of quinolone resistance are found in Campylobacter isolated from chicken (Gallus gallus) [12]. Fluoroquinolones are categorized as critically important drugs for human medicine by the WHO [13], and consequently Selleckchem Pifithrin�� surveillance programs to monitor trends in use [14]

and resistance [15,16,12] have been implemented. For Campylobacter, the principal molecular mechanisms of quinolone resistance consists in a single mutation C257T in the gyrA gene [17,18]. Consequently, PCR or sequenced-based methods targeting this quinolone resistance determining region (QRDR) have been shown to be highly predictive for detecting phenotypically resistant variants [16]. Moreover, previous work on gyrA suggested this locus might provide a host signature and thus be a good candidate for typing purposes [19,20]. The aims of this study were thus to evaluate the host specificity of the gyrA gene and to monitor quinolone resistance in a large Campylobacter jejuni and coli strain collection

originating from domesticated animals and surface water samples potentially contaminated by wildlife. Methods Isolates from non-human sources For this study, we characterized 430 C. jejuni and 280 C. coli isolated in Luxembourg from surface waters (SW), domesticated

mammals (DM) and poultry (P) between 2005 and 2012. Identification to the species selleck chemical level of the isolates was previously achieved buy Sirolimus by a duplex real-time PCR targeting the hipO gene of C. jejuni and a conserved region of the gyrA gene of C. jejuni and C. coli (outside the QRDR). Primer and probe combinations for the hipO Taqman-qPCR and gyrA FRET-qPCR systems were selected from published methods [21,22]. Real-time PCRs were performed using the FastStart DNA Masterplus HybProbe kit (Roche Diagnostic, Prophac, Luxembourg) in a total reaction volume of 20 μl containing the following final primer and probe concentrations: hipO primers 0.5 μM, hipO Taqman probe 0.1 μM, gyrA primers 1 μM and gyrA sensor and anchor probes 0.2 μM. The PCR programme included an initial activation step of 10 min at 95°C, 30 amplification cycles of 6 s at 95°C, 12 s at 54°C and 25 s at 72°C, followed by a melting curve analysis step of 1 min at 95°C, 50 s at 38°C, a rise to 80°C with an increase rate of 0.1°C s−1, and final cooling of 30 s at 40°C. C. jejuni and C. coli were identified by reading both the amplification and melting curves. Isolates with an atypical profile (i.e. hipO negative and a gyrA melting curve corresponding to no known species) were further confirmed as C.

The inhibition of c-FLIP expression can down-regulate HCC cell viability and up-regulate drug-induced cell apoptosis. Our data suggest that targeting c-FLIP in conjunction with anticancer therapies may have therapeutic potential by enhancing

HCC cell death. Acknowledgements This study was supported in part by a grant from National Natural Scince Foundation of China (No. 30700810). The authors would like to thank Dr Yi Wan(Department of medical statistics, FMMU, China) for his help with statistical work and Dr Haichao Wang(Chief, Basic Science Research Program, Department of Emergency Medicine, NSUH-NYU School of Medicine, Manhasset, NY) selleckchem for linguistic revision of the manuscript. References 1. Igney FH, Krammer PH: Death and anti-death: tumour resistance to apoptosis. Nat Rev Cancer 2002, 2: 277–88.CrossRefPubMed 2. Bouchet D, Tesson L, Ménoret S, Charreau B, Mathieu P, Yagita H, Duisit G, Anegon I: Differential sensitivity of endothelial cells of various species to apoptosis induced by gene transfer of Fas ligand: role of FLIP levels. Mol Med 2002, 8: 612–23.PubMed 3. Ishioka T, Katayama R, Kikuchi R, Nishimoto M, Takada S, Takada R, Matsuzawa S, Reed JC, Tsuruo T, Naito M: Impairment of the ubiquitin-proteasome system by cellular FLIP. Genes Cells 2007, 12: 735–44.PubMed 4. Rogers KM, Thomas M, Galligan L, Wilson TR, Allen WL, Sakai

H, Johnston PG, Longley DB: Cellular FLICE-inhibitory protein regulates chemotherapy-induced apoptosis in breast cancer cells. Mol Cancer Ther

2007, 6: 1544–51.CrossRefPubMed 5. Mezzanzanica D, Balladore E, Turatti F, Luison E, Alberti P, Bagnoli M, Figini M, Mazzoni A, Raspagliesi www.selleckchem.com/products/Trichostatin-A.html F, Oggionni M, Pilotti S, Canevari S: CD95-mediated apoptosis is impaired at receptor level by cellular FLICE-inhibitory protein (long form) in wild-type p53 human ovarian carcinoma. Clin Cancer Res 2004, 10: 5202–14.CrossRefPubMed 6. Hyer ML, Sudarshan S, Kim Y, Reed JC, Dong JY, Schwartz DA, Norris JS: Downregulation either of c-FLIP sensitizes DU145 prostate cancer cells to Fas-mediated apoptosis. Cancer Biol Ther 2002, 1: 401–6.PubMed 7. Krueger A, Baumann S, Krammer PH, Kirchhoff S: FLICE-inhibitory proteins: regulators of death receptor-mediated apoptosis. Mol Cell Biol 2001, 21: 8247–54.CrossRefPubMed 8. Kataoka T, Ito M, Budd RC, Tschopp J, Nagai K: Expression level of c-FLIP versus Fas determines susceptibility to Fas ligand-induced cell death in murine thymoma EL-4 cells. Exp Cell Res 2002, 273: 256–64.CrossRefPubMed 9. Irmler M, Thome M, Hahne M, Schneider P, Hofmann K, Steiner V, Bodmer JL, Schröter M, Burns K, Mattmann C, Rimoldi D, French LE, Tschopp J: Inhibition of death receptor signals by cellular FLIP. Nature 1997, 388: 190–5.CrossRefPubMed 10. Wilson TR, McLaughlin KM, McEwan M, Sakai H, Rogers KM, Redmond KM, Johnston PG, Longley DB: c-FLIP: A Key Regulator of Colorectal Cancer Cell Death. Cancer Res 2007, 67: 5754–62.CrossRefPubMed 11. Wajant H: Targeting the FLICE Inhibitory Protein (FLIP) in cancer therapy.

CrossRef 10. Ruiz AR, Gınsberg AL: Giant mesenteric hemangioma with small intestinal involvement: An unusual cause of recurrent gastrointestinal bleeding and review of gastrointestinal hemangiomas. Dig Dis Sci 1999, 12:2545–51.CrossRef 11. Corsi A, Ingegnoli A, Abelli P, De Chiara F, Mancini C, Cavestro GM, Fanigliulo L, Di Mario F, Franzi A, Zompatori M: Imaging of a small bowel cavernous VX-809 manufacturer hemangioma: Report of a case with emphasis on the use of computed tomography and enteroclysis. Acta Biomed 2007, 78:139–143.PubMed 12. Allred HW: Hemangiomas of the colon, rectum,

and anus. Mayo Clin Proc 1974, 49:739.PubMed 13. Lyon D, Mantia A: Large bowel hemangiomas. Dis Colon Rectum 1987, 27:404–14.CrossRef Competing interests The authors

declare that they have no competing interests. Authors’ contributions MK, MU and CI planned and wrote the manuscript. CI translated the manuscript to English. MU collected the datas. NO and FY performed the histopathologic evaluation. GE, MZ, MK and AC analyzed the present data and made the revisions.”
“The scenario sounds familiar. Last night I returned home very late after a full day of emergency surgeries. While I was having my usual cold dinner in front of the television with my entire family asleep, I received disturbing news; a famous Italian actor had undergone emergency surgery Selleckchem Belinostat in Honduras. the actor had been participating in a “”reality show”" and experienced severe back pain. For this reason, he was treated for one week with a NSAID. Suddenly, he developed acute abdominal pain and was taken to the nearest hospital. The diagnosis was acute appendicitis Morin Hydrate and he underwent immediate laparotomy via a Mc Burney

incision. Unfortunately, the surgeons were mistaken. The problem was a large perforated duodenal ulcer and the actor then underwent a midline incisioThe patient was subsequently transferred to a Miami acute care hospital. The story is always the same; we can call it emergency surgery, acute care surgery, or “”Samantha,”" but the key point is that we do not have a widespread set of minimum standards for emergency surgery. Such standards are just as important as those of ATLS. We need to develop guidelines regarding organizational models to address diseases requiring urgent surgical intervention. This is an integral component in the mission of the World Journal of Emergency Surgery and of the World Society of Emergency Surgery. We must be uniformly prepared all around the world, similar to the uniform emergency protocols for airplanes and airports. If we fail to meet this objective, we will continue to witness preventable complications and deaths affecting both the famous and the non-famous alike. This is a dream, but it needn’t be a broken one. In 2010 we will have the 1st World Congress of WSES. If we can successfully develop solid guidelines for surgeons from all around the world we will have accomplished a small yet important “”humanitarian mission.

The skin was washed

with 70% (v/v) ethanol and left to dry prior to wound creation. Excision wounds were created by pinching and lifting the skin of the back using sterile forceps and cutting a 6 mm circular (28 mm2) area using sharp BMS-354825 cell line scissors to cut down to the subcutaneous areolar tissue. Twenty-five μl of the bacterial suspension was then added to the wound (108 CFU of EMRSA-16), and incubated for one hour prior to treatment. MRSA was found to be the predominant bacterium colonising the wound at day 5 (data not included). Superficial wound model The preparation of the animals for this model was as described for the excisional wound model above. 25 mm2 square shaped wounds were created in the skin of the back by scarification using a 27G needle, run ten times parallel in one direction and another ten times perpendicular to the original tracks. The wounds were visibly red and mildly swollen after 30 minutes. Ten μl of the bacterial suspension was placed on the wound (4 × 107 CFU of EMRSA-16), and incubated for one hour prior to treatment. This method also resulted in a reproducible MRSA wound colonisation

model, which persisted for up to 5 days post inoculation (data not shown). Photodynamic therapy (PDT) All experiments were carried out under subdued room lighting. PDT was performed 1 hour after inoculating the wounds with the bacterial suspension. The excision wounds received 25 μl of MB (100 μg/ml) solely at the start of irradiation, whilst the superficial scarified wounds received 10 μl of MB just before the start of irradiation and a further 10 μl after 15 minutes of irradiation. The wounds were irradiated GSI-IX immediately after the application of MB and continued for 30 minutes. This equated to a total delivered light dose of 360 J/cm2. Following the completion of treatment, a circular area of skin and associated subcutaneous tissue of 1 cm diameter with the wound at its centre, was removed using sterile scissors. These were then placed

in 0·5 ml Stuart’s transport medium and shielded from light until Dapagliflozin delivery to the microbiology laboratory for processing and analysis within 2 hours. The animals were subsequently culled in accordance with the Animal Scientific Procedures act (1986). Control groups were used to test the effect of MB alone (by incubating wounds in the dark for the equivalent time period as needed for irradiation, L-S+, where L denotes light treatment and S denotes photosensitiser), light alone (by illuminating wounds in the absence of MB, L+S-). A final untreated control group received no MB or light illumination (L-S-). PBS was used instead of MB in the control wounds that received no MB. Twelve mice per group were examined in the excision wound model, whereas 6 mice per group were used in the superficial scarified wound model. In preliminary experiments, the dose of MB (concentration and volume of solution) was optimised to achieve maximum bacterial kill.

Env Microbiol 2005, 7:969–980.CrossRef 36. Aguilera-Arreola MG, Hernández-Rodríguez C, Zúñiga G, Figueras MJ, Garduño RA, Castro-Escarpulli G: Virulence potential and genetic diversity of Aeromonas caviae, Aeromonas veronii, and Aeromonas hydrophila clinical isolates from Mexico and Spain: a comparative JQ1 cost study. Can J Microbiol 2007, 53:877–887.PubMedCrossRef

37. Sneath PHA: Evidence from Aeromonas for genetic crossing-over in ribosomal sequences. Int J Syst Bacteriol 1993, 43:626–629.PubMedCrossRef 38. Morandi A, Zhaxybayeva O, Gogarten JP, Graf J: Evolutionary and diagnostic implications of intragenomic heterogeneity in the 16 S rRNA gene in Aeromonas strains. J Bacteriol 2005, 187:6561–6564.PubMedCrossRef 39. Umelo E, Trust TJ: Physical map of the chromosome of Aeromonas salmonicida and genomic comparisons between Aeromonas strains. Microbiol 1998,144(8):2141–2149.CrossRef

40. Georgiades K, Raoult D: Defining pathogenic bacterial species in the genomic era. Front Microbiol 2010, 1:151.PubMed 41. Martinez-Murcia AJ, Benlloch S, Collins MD: Phylogenetic interrelationships of members of the genera Aeromonas and Plesiomonas as determined by 16 S ribosomal DNA sequencing: Lack of congruence with results of DNA-DNA hybridizations. Int J Syst Bacteriol PI3K inhibitor 1992, 42:412–421.PubMedCrossRef 42. Huys G, Kämpfer P, Swings J: New DNA-DNA hybridization and phenotypic data on the species Aeromonas ichthiosmia and Aeromonas allosaccharophila: A. ichthiosmia Schubert et al. 1990 is a later synonym of A. veronii Hickman-Brenner et al. 1987. Syst Appl Microbiol 2001, 24:177–182.PubMedCrossRef 43. Nhung PH, Hata H, Ohkusu K, Noda M, Shah MM, Goto K, Ezaki T: Use of the novel phylogenetic Celastrol marker dnaJ and DNA-DNA hybridization to clarify interrelationships within the genus Aeromonas. Int J Syst Evol Microbiol 2007, 57:1232–1237.PubMedCrossRef 44. Saavedra MJ, Perea V, Fontes MC, Martins C, Martínez-Murcia A: Phylogenetic identification of Aeromonas strains isolated from carcasses of

pig as new members of the species Aeromonas allosaccharophila. Antonie Van Leeuwenhoek 2007, 91:159–167.PubMedCrossRef 45. Miñana-Galbis D, Urbizu-Serrano A, Farfán M, Fusté MC, Lorén JG: Phylogenetic analysis and identification of Aeromonas species based on sequencing of the cpn60 universal target. Int J Syst Evol Microbiol 2009, 59:1976–1983.PubMedCrossRef 46. Vial L, Chapalain A, Groleau M, Déziel E: The various lifestyles of the Burkholderia cepacia complex species: a tribute to adaptation. Env Microbiol 2011, 13:1–12.CrossRef 47. Monfort P, Baleux B: Dynamics of Aeromonas hydrophila, Aeromonas sobria and Aeromonas caviae in a sewage treatment pond. Appl Env Microbiol 1990, 56:1999–2006. 48. Goñi-Urriza M, Capdepuy M, Arpin C, Raymond N, Caumette P, Quentin C: Impact of an urban effluent on antibiotic resistance of riverine Enterobacteriaceae and Aeromonas spp. Appl Env Microbiol 2000, 66:125–132.CrossRef 49.

Details of the operating parameters of the arc discharge methane decomposition process are provided in Table 1. Table 1 Operating parameters of carbon strands Parameter Value Temperature At room environment Frequency 50 Hz High voltage 1 to 26 kV Flow rate 200 to 800 ppm Precursor DNA Synthesis inhibitor gas Pure methane (99.99%) Pressure Atmospheric Diagnostics of the carbon film Once the arc discharge is initiated, methane decomposition starts causing the resultant carbon atoms to deposit and stack up between the two electrodes creating a conductive bridge. The growth time was measured to be 11.6 s

at the voltage of 16.4 kV. The carbon film fabricated in this process is inspected using high-resolution optical microscopy, as shown in Figure 2. There are three configurations for installing the electrodes on the PCB board, namely, plane to plane (PTP), tip to plane (TTP), and tip to tip (TTT); however, in this study, we have only investigated the TTT structure.

Figure 2 TTT electrode configuration (a) before arc discharge decomposition, (b) carbon film obtained. Inspection by scan electron microscopy A scanning electron microscope (SEM) scans the samples with a focused beam of electrons. As the electrons collide with the atoms in the sample, they produce various signals which can be detected and measured [18]. These signals provide information about the surface topography and composition Wnt inhibitor of the sample. Microphotographic images from SEM have been provided in Figure 3a,b,c,d. Figure 3 SEM image of a sample. Imaging Non-specific serine/threonine protein kinase mode (a) × 370 at 15 kV, (b) × 1,500 at 10 kV, (c) × 4,000 at 15 kV, and (d) × 14,000 at 10 kV. Among all types of carbon allotropes, only graphene, graphite, and CNTs show electrical

conductivity. On the other hand, the carbon films also show conducting behavior. This implies that the grown carbonaceous materials belong to one of the above types of graphitized carbon. With reference to similar images from carbon materials published in the literature [19–21], it can be observed by comparison that the scanned material is composed of carbon. Results of optical emission spectroscopy The optical emission during arc discharge decomposition was captured in the wavelengths ranging from 385 to 750 nm through a spectrophotometer (StellarNet, Tampa, FL, USA), and the data of the recorded spectra was sketched using MATLAB software. Three evolved peaks of methane species were prominent which belong to CH, C2, and Hα as shown in Figures 4 and 5. As illustrated in Figure 4, the spectrum consists of the evolved phase of ionized species of methane which indicates peaks of CH at 397 and 431 nm, swan band C2 appearing at 516.75, and hydrogen Hα appearing at 657.33 nm.

MH, NR, and GS conceived and designed this study. NR and GS also supervised the project, participated in the discussion on the results, and helped improve the manuscript. All authors read and improved the final manuscript.”
“Background Detection of DNA sequences through hybridization between two complementary single strands is a basic method that is very often exploited at the DNA biosensor development [1]. Now new opportunities have appeared in this route due to synthesis of new nanomaterials which are intensively applied

as the scaffold, transducer, or sensitive detectors. In particular, carbon nanotubes have attracted keen interest of biosensor researchers [2]. GSK1120212 datasheet It was found that single-stranded nucleic acid (ssDNA) binds to the single-walled carbon nanotube (SWNT), forming a stable soluble hybrid in water [3]. In spite of the essential difference in CRM1 inhibitor structures of nanotubes and the biopolymer, ssDNA wraps tightly around the nanotube in water when hydrophobic nitrogen bases are adsorbed onto the nanotube surface via π-π stacking, while the hydrophilic sugar-phosphate

backbone is pointed towards water [3, 4]. The hybridization of nucleic acids on SWNT is extensively investigated [5–22], having in sight the development of DNA-hybridized biosensors on the base of nanotubes. Nevertheless, in spite of 10-year investigations in this field, some questions arise upon the study of DNA hybridization on the nanotube especially when the probe polymer was adsorbed to the tube surface directly. One of the keen questions is the effect of DNA interaction with the tube surface on the polymer hybridization. Effective Protein kinase N1 detection of hybridization of two complementary DNA strands on the nanotube surface was demonstrated in [5–7]; however, in other measurements [12,

14, 17], it was indicated that SWNT hampers effective hybridization of two polymers because of the strong interaction with the nanotube surface, which prevents the necessary conformational mobility of the polymer to be hybridized. Some researchers suppose that the double-stranded DNA (dsDNA) is desorbed from the sidewall of SWNT after hybridization [14, 18–22]. Thus, up to now, the full picture of the biopolymer hybridization on SWNT surface is still unclear, and in some cases, the conclusions are controversial. To clarify this ambiguity, an additional study is required. In this work, we focus our research on the hybridization of polyribocytidylic acid (poly(rC)) adsorbed to the carbon nanotube surface with polyriboinosinic acid (poly(rI)) free in solution.

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G: Evidence of crossprotection within Leptospira interrogans in an experimental model. Vaccine 2000, 19 (1) : 86–94.PubMedCrossRef 31. Goldsby R, Kindt TJ, Osborne BA, Janis K: Antigens. In Immunology. 5th edition. New York: W. H. Freeman and Company; 2003:57–75. 32. Wang LF, Yu M: Epitope identification and discovery using phage display libraries: applications in vaccine development and diagnostics. Curr Drug Targets 2004, 5 (1) : 1–15.PubMedCrossRef 33. Conway JF, Watts NR, Belnap DM, Cheng N, Stahl SJ, Wingfield PT, Steven AC: Characterization of a conformational Phospholipase D1 epitope on hepatitis B virus core antigen and

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