(DOC 430 KB) References 1 Pomeranz LE, Reynolds AE, Hengartner C

(DOC 430 KB) References 1. Pomeranz LE, Reynolds AE, Hengartner CJ: Molecular biology of pseudorabies virus: impact on neurovirology and veterinary medicine. Selleck GW786034 Microbiol Mol Biol Rev 2005,69(3):462–500.CrossRefPubMed

2. Roizman B, Pellett PE: The family Herpesviridae: a brief introduction. Fields virology 4 Edition (Edited by: Knipe DM, Howley PM). Philadelphia, Pa: Lippincott Williams & Wilkins 2001, 2:2381–2397. 3. Taddeo B, Esclatine A, Roizman B: The patterns of accumulation of cellular RNAs in cells infected with a wild-type and a mutant herpes simplex virus 1 lacking the virion host shutoff gene. Proceedings of the National Academy of Sciences of the United States of America 2002,99(26):17031–17036.CrossRefPubMed 4. Jones JO, Arvin AM: Microarray analysis of host cell gene transcription in response to varicella-zoster virus infection of human T cells and fibroblasts in vitro and SCIDhu skin xenografts in vivo. Journal of virology 2003,77(2):1268–1280.CrossRefPubMed 5. Ray N, Enquist LW: Transcriptional response of a common permissive cell type to infection by two diverse alphaherpesviruses. Journal of virology 2004,78(7):3489–3501.CrossRefPubMed 6.

Paulus C, Sollars PJ, Pickard GE, Enquist LW: Transcriptome signature of virulent and attenuated pseudorabies virus-infected rodent brain. Journal of virology 2006,80(4):1773–1786.CrossRefPubMed 7. Poletto R, Siegford ARN-509 solubility dmso JM, Steibel JP, Coussens PM, Zanella AJ: Investigation of changes in

global gene expression in the frontal cortex of early-weaned and socially isolated piglets using microarray and quantitative real-time RT-PCR. Brain reNCT-501 order search 2006,1068(1):7–15.CrossRefPubMed PD184352 (CI-1040) 8. Brittle EE, Reynolds AE, Enquist LW: Two modes of pseudorabies virus neuroinvasion and lethality in mice. Journal of virology 2004,78(23):12951–12963.CrossRefPubMed 9. Allison DB, Cui X, Page GP, Sabripour M: Microarray data analysis: from disarray to consolidation and consensus. Nature reviews 2006,7(1):55–65.CrossRefPubMed 10. Petalidis L, Bhattacharyya S, Morris GA, Collins VP, Freeman TC, Lyons PA: Global amplification of mRNA by template-switching PCR: linearity and application to microarray analysis. Nucleic acids research 2003,31(22):e142.CrossRefPubMed 11. Sykacek P, Furlong RA, Micklem G: A friendly statistics package for microarray analysis. Bioinformatics (Oxford, England) 2005,21(21):4069–4070.CrossRef 12. Wernisch L, Kendall SL, Soneji S, Wietzorrek A, Parish T, Hinds J, Butcher PD, Stoker NG: Analysis of whole-genome microarray replicates using mixed models. Bioinformatics (Oxford, England) 2003,19(1):53–61.CrossRef 13. Altschul SF, Gish W, Miller W, Myers EW, Lipman DJ: Basic local alignment search tool. Journal of molecular biology 1990,215(3):403–410.PubMed 14. Khatri P, Draghici S, Ostermeier GC, Krawetz SA: Profiling gene expression using onto-express. Genomics 2002,79(2):266–270.CrossRefPubMed 15.

Statistical Analysis Area under the curve (AUC) was calculated fo

Statistical Analysis Area under the curve (AUC) was calculated for each biochemical variable for both conditions using the trapezoidal method (AUCG) as described Dasatinib datasheet in detail by Pruessner et al. [18].

Statistical comparisons for biochemical (AUCG) and metabolic data were made between conditions using t-tests. Biochemical data, in addition to heart rate and blood pressure data, were also compared using a 2 (condition) × 4 (time) analysis of variance (ANOVA). Tukey’s post hoc tests were used where appropriate. All analyses were performed using JMP statistical software (version 4.0.3, SAS Institute, Cary, NC). Statistical significance was set at P ≤ 0.05. The data are presented as mean ± SEM, except for AZD0156 mw subject descriptive characteristics (mean ± SD). Results All subjects successfully completed all aspects of the study. AUC was greater for the dietary supplement compared to the placebo for NE (Figure 2B; p = 0.03), glycerol (Figure 3A; p < 0.0001), and FFA (Figure 3B; p = 0.0003). No difference was noted between conditions for EPI (Figure 2A; p > 0.05). For all variables, values were highest at 90 minutes post ingestion. When performing the 2 × 4 ANOVA for biochemical variables, a condition main effect was noted for NE (p < 0.0001), with no time effect (p = 0.13) or interaction

noted (p = 0.25). A condition main effect was noted for EPI (p = 0.04), with no time effect (p = 0.09) or interaction noted (p = 0.36). An

CHIR-99021 mw interaction was noted for glycerol (p = 0.0006), with values higher for supplement compared to placebo at 30, 60, and 90 minutes post ingestion Molecular motor (p < 0.05), and higher for supplement at all times post ingestion compared to pre ingestion (p < 0.05). A condition main effect was noted for FFA (p = 0.0003), with no time effect (p = 0.08) or interaction noted (p = 0.32). Total kilocalorie expenditure during the 30 minute collection period was 29.6% greater (p = 0.02) for the dietary supplement compared to placebo (Figure 4A). No difference was noted between conditions for respiratory exchange ratio (Figure 4B; p > 0.05). A condition main effect was noted for systolic blood pressure (p = 0.04), with values increasing from 117 ± 2 mmHg to 123 ± 2 mmHg with the dietary supplement, while remaining unchanged for placebo. No other hemodynamic changes were noted (p > 0.05). Hemodynamic data are presented in Table 2. Figure 2 Plasma epinephrine (A) and norepinephrine (B) data for 10 men consuming Meltdown ® and placebo in a randomized cross-over design. Data are mean ± SEM. * Greater norepinephrine AUC for Meltdown® compared to placebo (p = 0.03). Figure 3 Plasma glycerol (A) and free fatty acid (B) data for 10 men consuming Meltdown ® and placebo in a randomized cross-over design. Data are mean ± SEM. * Greater glycerol (p < 0.0001) and FFA (p = 0.0003) AUC for Meltdown® compared to placebo.

The ratio χ 1/χ 0 = O(c 2 u 2) < < 1, therefore, the nonlinear pa

The ratio χ 1/χ 0 = O(c 2 u 2) < < 1, therefore, the nonlinear parameter χ 1 can be neglected. The

CHIR98014 research buy statement about linearity of the ST-force agrees also with our simulations and the micromagnetic simulations performed in [12, 19]. The coefficient λ(J) describes nonlinearity of the system and decreases smoothly with the current J increasing. Numerical method We have simulated the vortex motion in a single permalloy (Fe20Ni80 alloy, Py) circular nanodot under the influence of a spin-polarized dc current flowing through it. Micromagnetic simulations of the spin-torque-induced magnetization dynamics in this system were carried out with the micromagnetic simulation package MicroMagus (General Numerics Research Lab, Jena, Germany) [28]. This package solves numerically the LLG equation of the magnetization motion using the optimized version of the adaptive (i.e., with the time step control) Runge-Kutta method. Selleckchem Lenvatinib Thermal fluctuations have been neglected in our modeling, so that the simulated dynamics corresponds to T = 0. Material parameters for Py are as follows: exchange Ruxolitinib mw stiffness constant A = 10-6

erg/cm, saturation magnetization M s = 800 G, and the damping constant used in the LLG equation α G  = 0.01. Permalloy dot with the radius R = 100 nm and thickness L = 5, 7, and 10 nm was discretized in-plane into 100 × 100 cells. No additional discretization was performed in the direction perpendicular Protein Tyrosine Kinase inhibitor to the dot plane, so that the discretization cell size was 2 × 2 × L nm3. In order to obtain the vortex core with a desired polarity (spin polarization direction of dc current and vortex core polarity should have opposite directions in order to ensure the steady-state vortex precession) and to displace the vortex core from its equilibrium position in the nanodot

center, we have initially applied a short magnetic field pulse with the out-of-plane projection of 200 Oe, the in-plane projection H x  = 10 Oe, and the duration Δt = 3 ns. Simulations were carried out for the physical time t = 200 to 3,000 ns depending on the applied dc current because for currents close to the threshold current J c1, the time for establishing the vortex steady-state precession regime was much larger than for higher currents (see Equation 8 below). Results and discussion Calculated analytically, the vortex core steady orbit radius in circular dot u 0(J) as a function of current J is compared with the simulations (see Figure 1). There is no fitting except only taking the critical current J c1 value from simulations.

52 mg of fluorescent product per mL of suspension, while in NC-RS

52 mg of fluorescent product per mL of suspension, while in NC-RS100 and in NC-S100, the liquid portion was 333 μL/10 mL of suspension corresponding to approximately 3.15 mg of fluorescent product per mL of suspension. It is important to note that the amount of rhodamine-labeled triglyceride can be increased or decreased, according to the needs of the study. The pH of the nanocapsule formulations (Table 1) was slightly acid and similar to the values previously reported for formulations prepared without the fluorescent-labeled oil [26, 29]. The size distribution profiles (Figure 5) and the D 4.3, SPAN, z-average, selleckchem PDI, and zeta potential values

for the formulations containing the fluorescent product 1 (Table 1) did not differ considerably from those observed for non-fluorescent formulations [25–27]. The zeta potential values for the formulations prepared with the fluorescent product 1 (Table 1) showed values approximately closed to those previously reported for the similar formulations prepared without the dye-labeled oil [25–27]. The electroPLX3397 price kinetic behavior of colloids is NU7441 cost related to the movement of ionic solutions near charged interfaces [30]. The carboxylic acids, as pendant groups in Eudragit S100 or as terminal groups

in PCL116, are in an acid-base balance at the particle-water interface producing carboxylate functions that react with NaCl forming the electrical double layer responsible for the eletrokinetic behavior of NC-S100 and LNC-PCL. On the other hand, the NC-RS has a polymer wall of poly(ethyl acrylate-co-methyl methacrylate-co-trimethylammonioethyl methacrylate chloride), whose monomer units are at 1:2:0.1 proportions. In this way, the trimethylammonioethyl moiety has a quaternary nitrogen giving to the particle-water interface a positive charge. The electrokinetic properties of NC-RS are related to the positive surface potential that those nanocapsules present after dilution

in 10 mmol L-1 NaCl aqueous solution. Considering that all formulations contain polysorbate 80, the mechanism of stabilization of those colloids is not exclusively based Selleckchem Forskolin on the electrical repulsion of the particles since the steric hindrance effect of the surfactant plays an important role [31–33]. Then, even though the zeta potential values are near zero for all formulations, the colloidal turbid solutions have an adequate kinetic stability for the purpose of drug delivery. The NC-RS100 and NC-S100 formulations presented higher concentrations of particles (approximately 1.7-fold and 1.4-fold, respectively) than LNC-PCL (P < 0.05). This result was expected since the volumetric fraction of the dispersed phase in these formulations is higher than that of LNC-PCL, and the z-average values obtained for each formulation were similar [8]. The fluorescence spectroscopy analysis of the fluorescent nanocapsules and fluorescent lipid-core nanocapsules showed that the fluorescence property is maintained after the preparation of these formulations (Figure 6).

J Bacteriol 2006,188(21):7707–7710 CrossRefPubMed 36 Yura T: Reg

J Bacteriol 2006,188(21):7707–7710.CrossRefPubMed 36. Yura T: Regulation and conservation of the heat-shock transcription factor sigma 32. Genes Cells

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and Burkholderia cenocepacia. Int J Immunophatol Pharmacol 2005,18(4):661–170. 40. Heymann P, Gerads M, Schaller M, Dromer F, Winkelmann G, Ernst JF: The siderophore iron transporter of Candida albicans (Sit1p/Arn1p) mediates uptake of ferrichrome-type siderophores and is required for epithelial invasion. Infect Immun 2002,70(9):5246–5255.CrossRefPubMed 41. Foster SL, Richardson SH, Failla ML: Elevated iron status increases bacterial invasion and survival and alters Elafibranor cytokine/chemokine mRNA expression in Caco-2 human intestinal cells. J Nutr 2001,131(5):1452–1458.PubMed 42. Ermolaeva MD, White O, Salzberg SL: Prediction of operons in microbial genomes. Nucleic Acids Teicoplanin Res 2001,29(5):1216–1221.CrossRefPubMed 43. Lestrate P, Dricot A, Delrue RM, Lambert C, Martinelli V, De Bolle X, Letesson JJ, Tibor A: Attenuated signature-tagged mutagenesis see more mutants of Brucella melitensis identified during the acute phase of infection in mice. Infect Immun 2003,71(12):7053–7060.CrossRefPubMed 44. Gallot-Lavallee T, Zygmunt MS, Cloeckaert A, Bezard G, Dubray G: Growth phase-dependent variations in the outer membrane protein profile of Brucella melitensis. Res Microbiol 1995,146(3):227–236.CrossRefPubMed 45. Uzureau S,

Godefroid M, Deschamps C, Lemaire J, De Bolle X, Letesson JJ: Mutations of the quorum sensing-dependent regulator VjbR lead to drastic surface modifications in Brucella melitensis. J Bacteriol 2007,189(16):6035–6047.CrossRefPubMed 46. Delrue RM, Lestrate P, Tibor A, Letesson JJ, De Bolle X:Brucella pathogenesis, genes identified from random large-scale screens. FEMS Microbiol Lett 2004, 231:1–12.CrossRefPubMed 47. Godfroid F, Taminiau B, Danese I, Denoel P, Tibor A, Weynants V, Cloeckaert A, Godfroid J, Letesson JJ: Identification of the perosamine synthetase gene of Brucella melitensis 16 M and involvement of lipopolysaccharide O side chain in Brucella survival in mice and in macrophages. Infect Immun 1998,66(11):5485–5493.PubMed 48. Haine V, Sinon A, Van Steen F, Rousseau S, Dozot M, Lestrate P, Lambert C, Letesson JJ, De Bolle X: Systematic targeted mutagenesis of Brucella melitensis 16 M reveals a major role for GntR regulators in the control of virulence.

PubMedCrossRef 18 Monden T, Nakamura H, Murai A: The sugar compo

PubMedCrossRef 18. Monden T, Nakamura H, Murai A: The sugar composition and partial structure of the self-induced endogenous elicitor from potato. Biochem Biophys

CYC202 order Res Commun 1995,215(2):768–773.PubMedCrossRef 19. Davis KR, Lyon GD, Darvill AG, Albersheim P: Host-pathogen interactions: XXV. Endopolygalacturonic acid lyase from Erwinia carotovora elicits phytoalexin accumulation by releasing plant cell wall fragments. Plant Physiol 1984,74(1):52–60.PubMedCrossRef 20. Nothnagel EA, McNeil M, Albersheim P, Dell A: Host-pathogen interactions: XXII. A galacturonic acid oligosaccharide from plant cell walls elicits phytoalexins. Plant Physiol 1983,71(4):916–926.PubMedCrossRef 21. Cabrera JC, Boland A, Messiaen J, Cambier P, Van Cutsem P: Egg box conformation of oligogalacturonides: the time-dependent stabilization of the elicitor-active conformation increases its biological activity. Glycobiology 2008,18(6):473–482.PubMedCrossRef 22. Kohorn BD, Johansen S, Shishido A, Todorova T, Martinez R, Defeo E, Obregon P: Pectin activation of MAP kinase and gene expression is WAK2 dependent. Plant J 2009,60(6):974–982.PubMedCrossRef 23. Brutus A, Sicilia F, Macone A, Cervone F, De Lorenzo G: A domain swap

approach reveals a role of the plant wall-associated kinase 1 (WAK1) as a receptor of oligogalacturonides. Proc Natl Acad Sci USA 2010,107(20):9452–9457.PubMedCrossRef 24. Xanthomonas. Chapman & Hall, London; 1993. 25. Alvocidib chemical structure Ryan RP, Vorhölter FJ, Potnis N, Jones JB, Van Sluys MA, Bogdanove AJ, Dow JM: Pathogenomics of Xanthomonas: understanding bacterium-plant interactions. Nat Rev Microbiol 2011,9(5):344–355.PubMedCrossRef

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The absorptance values were analyzed using one-way ANOVA and the

The absorptance values were analyzed using one-way ANOVA and the differences between the cells that stably expressing shGRP78-3 and control cells were significant (p < 0.05), suggesting that GRP78 knockdown decreased the expression levels of MMP-2, MMP-9, MMP-14 and TIMP-2 in SMMC7721 cells (Figure 4B and 4C). We further analyzed whether Grp78 knockdown affected the activity of MMP2 and MMP9 by gelatin-zymography assay. As shown in Figure 4D and 4E, the

activity Trichostatin A manufacturer of MMP-2 in C3 and C4 cells was significantly lower than that in parental and vector transfected cells, The absorptance values were analyzed by one-way ANOVA and the differences between the cells that stably expressing shGRP78-3 and control cells were significant (p < 0.05). However, we do not detect the activity of MMP-9 in parental, vector, C3 and C4 cells. Taken together, our findings demonstrate that GRP78 knockdown inhibites the ECM degradation by decreasing the expression and activity of MMP-2. Figure 4 GRP78 knockdown decreased ECM degradation. (A) FITC-gelatin degradation analysis of the extracellular matrix degradation capability of the cells that stably expressing shGRP78-3.

The experiments were repeated for three times. (B) Western blot analysis of MMP-2,MMP-9,MMP-14 and TIMP-2 expression in the cells that stably expressing shGRP78-3, and the results of quantative analysis were represented as ± SE and analyzed by one-way ANOVA (Columns,mean of three separate experiments; bars, SE; *, values significantly different at the 5% levels). (C) and (D) Gelatin zymograph analysis of the MEK162 activities PS-341 clinical trial of MMP-2 and MMP-9 in GRP78 knockdown cells. The activities of MMP-2 and MMP-9 were represented as ± SE and analyzed by one-way ANOVA (Columns,mean of three separate experiments; bars, SE; *, values significantly different at the 5%

levels). GRP78 knockdown decreased JNK and ERK signaling pathway We then sought to determine the mechanisms underlying the reduction of MMPs activities caused by GRP78 knockdown in SMMC7721 cells. For the important roles of ERK1/2 and JNK in the regulation of MMP-2 and MMP-9 activities, we examined the phosphorylation Montelukast Sodium levels of ERK1/2 and JNK in C3 and C4 cells using western blot. As shown in Figure 5A and B, the p-ERK1/2 and p-JNK levels were reduced as compared with control cells. The values were analyzed by one-way ANOVA and the differences between C3 or C4 cells and control cells were significant (p < 0.05). Because the activities of ERK1/2 and JNK were modulated in large part by FAK-Src signaling pathway [22], we examined the phosphorylation levels of FAK at Y397 and Src at Y416 in C3 and C4 cells. We found that GRP78 knockdown significantly decreased the levels of pY397-FAK and pY416-Src in SMMC7721 cells (p < 0.05) (Figure 5C).

CrossRefPubMed 12 Korkolopoulou P, Saetta AA, Levidou G, Gigelou

CrossRefPubMed 12. Korkolopoulou P, Saetta AA, Levidou G, Gigelou F, Lazaris A, Thymara I, Scliri M, Bousboukea K, Michalopoulos NV, Apostolikas N, Konstantinidou A, Tzivras M, Patsouris E: c-FLIP expression in colorectal carcinomas: association with Fas/FasL expression and prognostic implications. Histopathology 2007, 51: 150–6.CrossRefPubMed 13. Brummelkamp TR, Bernards R, Agami R: A system for stable expression of short interfering RNAs in mammalian cells. Science 2002, 296: 550–3.CrossRefPubMed

14. Flahaut M, Mühlethaler-Mottet A, Auderset K, Bourloud KB, Meier R, Popovic MB, Joseph JM, Gross N: Persistent inhibition of FLIP(L) expression by lentiviral small hairpin RNA delivery restores death-receptor-induced apoptosis in neuroblastoma cells. Apoptosis 2006, 11: 255–63.CrossRefPubMed CB-839 15. Grigioni WF, D’Errico A, Bacci F, Gaudio M, Mazziotti A, Gozzetti G, Mancini AM: Primary liver neoplasms: evaluation of proliferative index using MoAb Ki-67. J Pathol 1989, 158: 23–9.CrossRefPubMed 16. Yang X, Khosravi-Far R, Chang HY, Baltimore D: Daxx, a novel Fas-binding protein that activates JNK and apoptosis. Cell 1997, 89: 1067–76.CrossRefPubMed 17. Jäckel MC: Genetic AG-120 in vivo control of programmed cell death (apoptosis): prospects for biological tumor staging? HNO 1998, 46: 614–25.CrossRefPubMed 18. Okano H, Shiraki K, Inoue H, Kawakita T, Yamanaka T, Deguchi M, Sugimoto K, Sakai T, Ohmori S, Fujikawa K, Murata K, Nakano T: Cellular

FLICE/caspase-8-inhibitory Ibrutinib price protein as a principal regulator of cell death and survival in human hepatocellular carcinoma. Lab Invest 2003, 83: 1033–43.CrossRefPubMed 19. Kataoka T, Budd RC, Holler N, Thome M, Martinon F, Irmler M, Burns K, Hahne M, Kennedy N, Kovacsovics M, Tschopp J: The caspase-8 inhibitor FLIP PLX4032 mouse promotes activation of NF-kappaB and Erk signaling pathways. Curr Biol 2000, 10: 640–8.CrossRefPubMed 20. Kreuz S, Siegmund D, Scheurich P, Wajant H: NF-kappaB inducers upregulate cFLIP, a cycloheximide-sensitive

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The dried biofilms were mounted on metal specimen stubs, coated w

The dried biofilms were mounted on metal specimen stubs, coated with a 16 nm thick platinum film, and imaged using an XL-30 S FEG SEM (FEI Company, Hillsboro, OR) operating at 5 kV. Transmission electron microscopy (TEM) Bacterial biofilms (1 to 3 weeks old cultures, depending on the experiment) were immobilized by rapid freezing [56], dehydrated by freeze-substitution in cold acetone containing glutaraldehyde (1% v/v, from a 10% stock solution in acetone; EMS Hatfield, PA) and osmium tetroxide (1% w/v) [57–59] and embedded in resin. Rapid freezing was achieved either by using a high-pressure freezer (EMPACT2 HPF, Leica Microsystems, Inc, Deerfield,

IL) or by immersion in liquid propane. Thin sections were prepared from different regions of the embedded Selleckchem Wortmannin specimen blocks, stained with uranyl acetate and lead citrate, and were examined in a TEM (CM 120 BioTwin, FEI, Inc., Hillsboro, OR). Biofilm chemical analysis Supernatant spent media was decanted from biofilms (1 week old culture) at the bottom of the culture tubes. A glass Pasteur pipette was then used to aspirate the complete biofilm from the tube and collected in a 12 mm glass test tube. Biofilms from 17 culture tubes were combined in this fashion. Biofilm-free spent media (5 × 2 mL in 12 mm tubes) and the combined biofilm samples eFT-508 supplier were freeze-dried overnight in a SpeedVac concentrator (SVC100H, Savant, Thermo

Fisher Scientific, Inc., Waltham, MA) equipped with a refrigerated condensation trap. SDS-buffer consisting of 1 mM Tris/Tris HCl, 0.1 mM EDTA, 0.15 M NaCl, 1% w/v SDS with a final pH (unadjusted) of 7.51 at 25°C was used to dissolve freeze-dried biofilm/media samples (10 mg in 3 mL) with sonication until a pale yellow solution was obtained. Dry biofilm and media samples were analyzed for calcium and magnesium content by ICP-AES (Galbraith Laboratories, Inc., Knoxville, TN). IR absorption spectra were collected on an FTIR spectrometer (Magna-IR 560, Nicolet, Madison, WI) as 12 mm diameter discs using ca. 3 mg of dry sample in ca. 150 mg of potassium

bromide. UV spectra of the SDS-buffer solutions were BCKDHB obtained using a Model 8452A (Hewlett-Packard, Palo Alto, CA) diode array spectrophotometer in a 1 cm optical path with SDS-buffer as a reference. Total carbohydrate concentrations were measured as previously described [41, 60]. These measurements were carried out on suspensions of solid biofilm/media samples in DI-H2O because SDS-buffer interfered with the assay. Dextrose monohydrate in DI-H2O (21.3 mg in 100 mL) was used as a stock solution to prepare check details standards. The absorbances at 480 nm (acidic polysaccharides) and at 490 nm (neutral polysaccharides) were corrected with the absorbance at 600 nm. Protein and nucleic acid concentrations were estimated from the baselined UV spectra [61, 62].

5009113), a grant from the Program of Shenzhen Science and techno

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