GST+5335 elutions were also concentrated over Microcon 10,000 MWCO columns prior to use in shift assays. For a negative control, the purified recombinant protein HctEIVA from the hectochlorin pathway (purification described in [39]) was used. The concentrations of HctEIVA protein used in the EMSA experiments were measured using a Bradford assay, and the purified HctEIVA included a 6× N-terminal His tag from its expression vector (pET28b; Novagen). Each gel shift assay reaction was performed with the indicated quantities of DNA and purified protein (Figure 9) in EMSA

binding buffer adapted from the DIG Gel Shift Kit, 2nd generation protocol (Roche) [20 mM HEPES, pH 7.6, 1 mM EDTA, 10 mM (NH4)2SO4, 1 mM DTT, Tween 20, 0.2% (w/v), 30 mM KCl] and water (total volume 20 μl) for 30 min at room temperature. this website Following the incubation period, 5 μl of native loading dye containing bromophenol blue was check details added to each reaction, and the reaction contents were immediately transferred to a 10% native PAGE gel. The gels were electrophoresed at 85 V for ~3.0 h in 0.5× TBE buffer (44.5 mM Tris, 44.5 mM boric acid, 1 mM EDTA), followed by staining for at least 10 min in SYBR Gold Nucleic Acid Gel Stain (Molecular Probes/Invitrogen) and visualization find more on a UV transilluminator. Sequence information DNA and amino acid sequences of the proteins identified in this study have been deposited in Genbank

under the accession numbers GQ860962 and GQ860963. Acknowledgements The authors wish to thank Carla M. Sorrels for assistance with RNA extraction procedures, Sheila Podell for assistance with bioinformatics, and R. Cameron Coates and Tara Byrum for maintenance of JHB cultures. This work was supported by grants from the NIH (GM075832 and NS053398), and NOAA Grant Tau-protein kinase NA08OAR4170669, California SeaGrant College Program Project SG-100-TECH-N, through NOAA’s National Sea Grant College Program, US Department of Commerce.

The statements, findings, conclusions, and recommendations are those of the authors and do not necessarily reflect the views of California Sea Grant or the US Department of Commerce. Electronic supplementary material Additional file 1: Table S1: Primers used in this study. This Excel file (.xls) is a complete list of all primers used for RT-PCR experiments, β-galactosidase reporter assays, and protein identification, recombinant expression, and EMSA experiments. (XLS 27 KB) Additional file 2: Figure S1: Sequence alignment with Lyngbya majuscula JHB protein 7968 and 5 proteins with highest identity matches from NCBI BLAST analyses. This TIFF file (.tiff) shows an alignment of these 6 protein sequences performed in ClustalX2. (TIFF 379 KB) Additional file 3: Figure S2: EMSA with DNA region -1000 – -832 bp upstream of jamA and protein GST+5335. This TIFF file (.tiff) shows, from left to right: 270 fmol DNA only, 8.4 pmol, 16.4 pmol, 33.5 pmol, and 67.0 pmol of GST+5335 combined with 270 fmol DNA.

No significant differences in serum IgG, IgA, neutrophils and lymphocytes were observed among the three patterns, however, the intercept of the models was consistently significant (for all: P < 0.05), once corrected for variability between hosts and their multiple sampling. This finding supports the hypothesis that the strength find more of the initial immune response is crucial in modulating the dynamics of shedding. During the second week post infection, differences in

the dynamics of infection were observed between the intermittent and the fade-out group (no data were available for the non-shedding group). The relatively low number of bacteria shed by the intermittent group (mean CFU/sec. ± S.E.: 0.083 ± 0.019) was associated with low serum IgG (OD index ± S.E.: 0.238 ± 0.028) and high serum IgA (1.107 ± 0.052) as well as high circulating neutrophils (mean K/μL ± S.E.: 1.436 ± 0.158) and lymphocytes (mean K/μL ± S.E.: 2.150 ± 0.412). buy LY333531 In contrast, the higher shedding in

the fade out group (mean CFU/sec. ± S.E.: 0.213 ± 0.045) was correlated to high serum IgG (OD index ± S.E.: 0.434 ± 0.118) and low serum IgA (0.667 ± 0.128) and white blood cells (mean K/μL ± S.E., neutrophils: 0.896 ± 0.00 and lymphocytes: 0.740 ± 0.000). Although not conclusive or statistically significant, these relationships suggest that the strength of the early antibody and blood cells response may play a role in affecting both the initial and long-term pattern of B. bronchiseptica transmission. Host immune response overview Overall, the immune response of rabbits to B. bronchiseptica infection confirmed previous findings reported in other animal models [14–19, 25]. Peripheral response Infected hosts developed a strong serum

IgG and IgA response compared to the controls (Fig. 3). The level of IgG rapidly increased in infected rabbits and remained consistently high for the duration of the N-acetylglucosamine-1-phosphate transferase infection, however and as previously highlighted, it was not sufficient to completely clear the bacteria from the upper respiratory tract (interaction between INK1197 ic50 sampling time and infected-controls, coeff ± S.E.: 0.047 ± 0.005 d.f. = 328 P < 0.0001 -corrected for the random effect of the host and its longitudinal sampling). IgA levels in infected rabbits peaked around week three post infection and decreased thereafter, probably as a consequence of the successful clearance of bacteria from the lower respiratory tract [25, 26]. Nevertheless, values remained significantly higher in infected compared to controls (coeff ± S.E.: 0.208 ± 0.056 d.f. = 45 P < 0.001) and for the duration of the experiment (interaction between infected-controls and sampling time, coeff ± S.E.: 0.0026 ± 0.001 d.f. = 410 P < 0.01; corrected for the host variability). Collectively, the systemic antibody profiles suggest that rabbit immune protection against B.

Potential

arrangement variants are: arrangement as determined by genome sequencing [1], at least two head-to-tail copies of RD2, tail-to-tail, single copy arranged in reverse orientation than the integrative copy determined by genome sequencing, head-to-tail arrangement of copies in reverse orientation than the integrative copy determined by genome sequencing, head-to-head, and circular form. B. PCR screen detects product amplified Pexidartinib solubility dmso with primer pairs #1+#2, #3+#4, and #2+#3, corresponding to arrangement variant (head-to-tail) or (circular form), and #1+#4 detecting chromosomal integration site lacking RD2. C. Primers #2+#3 detect arrangement variant 2 or 7 in multiple RD2 positive strains [1]. Serotype M1 strain MGAS5005 (lacks RD2) was used as a negative control of amplification. To further investigate the putative presence of multiple extrachromosomal copies of RD2 in GAS cells, we performed quantitative real time PCR using total DNA isolated from MGAS6180 strain. Performed analysis revealed that RD2 is present in 6-9 copies per chromosome (Figure 5B, see below). Also,

the amplification of chromosomal junction (primers #1+#4) suggests that RD2 can be excised from the site of integration. Figure 5 Mitomycin C treatment results in amplification of RD2. A Rapid decrease in O.D. of a liquid culture of strain MGAS6180 after mitomycin C addition. The decreased O.D. is likely due to prophage induction followed by lytic cycle CH5183284 find more phage release. Smaller drop in OD is

observed after treatment with hydrogen peroxide. B. The RD2 element is present in 6-9 copies per chromosome in the absence of inducer. C. The RD2 element is not induced by oxidative stress. Bars in each group represent the RD2 copy number after 1 h, 2 h, 3 h, and 16 h after treatment with hydrogen peroxide. D. RD2 is induced by DNA damage. Bars in each group represent the increase in copy number at 1 h, 2 h, 3 h, and 16 h after treatment with mitomycin C. The statistical significance of the increase in RD2 copy number was determined by t-test, *** on the graph denotes p value below 0.001. Taken together, these results indicate that a circular form of RD2 is present in strain MGAS6180. Response of strain MGAS6180 to mitomycin C and hydrogen peroxide treatment We hypothesized that the putative circular form detected in overnight cultures (see above) is a transient form involved in DNA transfer. DNA damaging factors as ultraviolet light, hydrogen peroxide, or mitomycin C can induce mobilization of genetic elements such as prophages or pathogenic islands as part of a response to DNA selleck damage or oxidative stress [23]. To test hypothesis that RD2 was induced/excised by DNA damage and oxidative stress, we examined induction of RD2 and five other integrative elements present in the genome of strain MGAS 6180 by mitomycin C and hydrogen peroxide treatment.

In this setting, herb derived products are usually suggested because the high title of active principles promises results similar to those obtained with pharmaceutical drugs but in absence of side effects and without the risk of testing positive for doping. Among the “natural” supplements,

the most “attractive” are those containing plant-derived hormones such as ecdysteroids, phytoestrogens and vegetal sterols and other substances with referred hormone modulating properties such as tribulus Transmembrane Transporters inhibitor terrestris. Ecdysteroids are the steroid hormones of arthropods. They also occur in certain plant species, where they are known as phytoecdysteroids and are believed to contribute to the deterrence of invertebrate predators. In insects, they regulate moulting and metamorphosis and have GW-572016 order been implicated in the regulation of reproduction and diapause. Most actions of ecdysteroids are mediated by intracellular receptor complexes, which regulate gene expression in a tissue and development specific manner. Ecdysteroids are apparently non-toxic to mammals and a wide range of beneficial pharmacological (adaptogenic, anabolic, anti-diabetic, hepatoprotective, immunoprotective, wound-healing, and perhaps even anti-tumour) activities are claimed for them [6]. Moreover, the reported anabolic properties have led to a large (and unregulated) market for HKI-272 ic50 ecdysteroid-containing

preparations, the most of which are advertised on specialized websites as legally allowed and non-toxic substances useful to gain muscular mass [7]. Phytoestrogens have acquired popularity for a multitude Meloxicam of health benefits, including a lowered risk of osteoporosis, heart disease, breast cancer, and menopausal symptoms, that have been attributed to them. Consequently, a global movement towards increased consumption of phytoestrogen-rich foods and tabletized concentrated

isoflavone extracts have been heavily promoted in western countries over the last two decades. However, more recently, phytoestrogens have been considered endocrine disruptors having the potential to cause adverse health effects [8], as well the effects of phytoestrogens in preventing osteoporosis and menopausal symptoms have not been confirmed in more recent studies [9–11]. Phytosterols (including campesterol, stigmasterol and sitosterol) are plant steroids with a similar chemical structure and cellular function to human cholesterol. They are recommended as dietary modifiers of serum lipids [12]. In addition, plant sterols exert beneficial effects on other lipid variables, such as apolipoprotein (apo) B/apoAI ratio and, in some studies, high-density lipoprotein cholesterol (HDL-C) and triglycerides [13] and may also affect inflammatory markers, coagulation parameters, as well as platelet and endothelial function.

Aude Michel (PECSA, Université Pierre et Marie Curie, Paris, France) is also kindly acknowledged for the TEM

experiments. Electronic supplementary material Additional file 1: Supporting information. SI-1. Characterization of nanoparticle sizes and size distribution. SI-1.1.Vibrating sample magnetometry (VSM). SI-1.2. Transmission Electron Microscopy (TEM). SI-1.3. Dynamic Light Scattering (DLS). SI-2. Characterization of polymer coated nanoparticle. SI-2.1. Number of poly (acrylic acid) chains per particle. SI-2.2. Number of electrostatic charges borne by the PAA2K-coated particles. SI-3. Mixture of the oppositely charged wires of PEI. (DOC VX-689 ic50 602 KB) References 1. Dubin PL, The SS, IL Receptor inhibitor McQuigg DW, Chew CH, Gan LM: Binding of polyelectrolytes to oppositely charged ionic micelles at critical micelle surface charge densities. Langmuir 1989,5(1):89–95.CrossRef 2. Dubin PL, Curran ME, Hua J: Critical linear charge density for binding of a weak polycation to an anionic/nonionic mixed micelle. Langmuir 1990,6(3):707–709.CrossRef 3. McQuigg DW, Kaplan JI, Dubin click here PL: Critical conditions for the binding

of polyelectrolytes to small oppositely charged micelles. J Chem Phy 1992,96(4):1973–1978.CrossRef 4. Wen YP, Dubin PL: Potentiometric studies of the interaction of bovine serum albumin and poly(dimethyldiallylammonium chloride). Macromolecules 1997,30(25):7856–7861.CrossRef 5. Yoshida K, Dubin PL: Complex formation between polyacrylic acid and cationic/nonionic mixed micelles: effect of pH on electrostatic interaction and hydrogen bonding. Colloids Surf A Physicochem Eng Asp 1999,147(1–2):161–167.CrossRef 6. Seyrek E, Dubin PL, Staggemeier BA: Influence of chain stiffness on the interaction of polyelectrolytes with oppositely charged micelles and protein. J Phys Chem B 2003,107(32):8158–8165.CrossRef 7. Alexander S: Polymer adsorption on Protein kinase N1 small spheres. A scaling approach. J Phys France 1977,38(8):977–981.CrossRef 8. Pincus PA, Sandroff CJ, Witten TA: Polymer adsorption on colloidal particles. J Phys France 1984,45(4):725–729.CrossRef 9. Muthukumar M: Adsorption of a polyelectrolyte chain to

a charged surface. J Chem Phy 1987,86(12):7230–7235.CrossRef 10. Goeler FV, Muthukumar M: Adsorption of polyelectrolytes onto curved surfaces. J Chem Phy 1994,100(10):7796–7803.CrossRef 11. Kong CY, Muthukumar M: Monte Carlo study of adsorption of a polyelectrolyte onto charged surfaces. J Chem Phy 1998,109(4):1522–1527.CrossRef 12. Haronska P, Vilgis TA, Grottenmüller R, Schmidt M: Adsorption of polymer chains onto charged spheres: experiment and theory. Macromol Theor Simul 1998,7(2):241–247.CrossRef 13. Netz RR, Joanny J-F: Complexation between a semiflexible polyelectrolyte and an oppositely charged sphere. Macromolecules 1999,32(26):9026–9040.CrossRef 14. Schiessel H: Charged rosettes at high and low ionic strengths. Macromolecules 2003,36(9):3424–3431.CrossRef 15.

For many years this transition has been casually associated with the Isthmus of Kra (Fig. 1), which is actually 300 km further south at 10°30′N. Hughes et al. (2003) studied the avian Indochinese-Sundaic transition and found a significant turnover in bird species between 11°N and 13°N, just north of the Isthmus of

Kra; 152 species, or half the forest-associated species present regionally, have range limits in this area. In many genera, northern species are replaced with southern species with very little range overlap. In mammals, Woodruff and Turner (2009) also traced the transition to the northern third of the peninsula but, instead of a narrow zone of replacement near the Isthmus of Kra, they found (1) an area of the peninsula from 8–14°N with 30% fewer species than expected and (2) Indochinese and Sundaic species range limits clustered just north (14°N) and south (5°N) of this species richness anomaly. Elements of this pattern are NVP-HSP990 similar to those found independently by Cattulo et al. (2008). As in the plants, the faunal dissimilarity across the

mammal Indochinese-Sundaic transition is greater than that on either side of Wallace’s Line (Kreft and Jetz, in review). Comparable analyses of the magnitude and location of the zoogeographic transition in other phyla are still lacking but, as a broad generalization, reptiles, amphibians and butterflies exhibit similar patterns (references in Woodruff 2003a, b). The history of the Indochinese-Sundaic transition will be discussed more Galeterone Selleckchem VX-661 below. Biogeographic issues of relevance to conservation Documenting biogeographic patterns Any discussion of regional patterns must begin by noting the strengths and weaknesses in the underlying distributional database. Its great strengths lie in the richness of the species lists and the fact that observations of many taxa span 200 years. The two great weaknesses remain the geographic gaps in the survey work and the ad hoc nature of the

record keeping. Wars, insurgencies and inaccessibility prevented biological exploration of parts of the region for many years and survey work has been a low priority of regional governments. Parnell et al. (2003) HKI-272 in vitro provide an excellent quantification of the effects of collecting patterns on our knowledge of Thai plants. The probable extent of our ignorance is indicated by the description of hundreds of new species of vertebrates and plants in both Vietnam and central Borneo since 1992 (Sterling et al. 2006; World Wildlife Fund 2009). Similar surprises can be expected in Myanmar where the northern limits of the Sundaic biota cannot be considered known until the Tenasserim is surveyed. The other weakness in the regional distributional database is the lack of standardized record keeping at national levels. Although progress is being made (e.g., SAMD 2008; Scholes et al. 2008; GBIF 2009; Webb et al.

Figure 4 The activation profiles of macrophages treated with IFN-γ or IL-10 and infected with pathogenic mycobacteria. BMDM were pretreated, or not, with murine r-IFN-γ or r-IL-10 for 2 h, infected with the studied mycobacterial strains at a MOI of 5:1, washed, treated again with the cytokines and incubated for an additional 48 h. The cells stimulated with LPS and r-IFN-γ

for 48 h, or left untreated, were used as a positive and negative controls of classical proinflammatory activation, respectively. To evaluate markers of M1-type activation, the culture supernatants were tested for proinflammatory mediator levels (A-C) and the adhered cells were tested for expression of iNOS (D). Measurement of TNF-α, IL-6, MCP-1, MIP-2 and IL-12 concentrations was performed by Bioplex test, and Torin 1 research buy NO production was evaluated by Griess reaction Assays were completed with duplicate samples, and results are expressed as a mean of three independent experiments. To evaluate markers of M2-type activation, expression of Arginase 1 and MR/CD206 in the adhered cells was tested by Western blotting (E) and secretion of IL-10 was quantified by Bioplex assay (F). Lower panels in D and

E, quantification of the protein levels by densitometric analysis of immunoreactive bands. Asterisks in A, B and F indicate the infected cultures treated with recombinant IFN-γ or IL-10, for which the induced cytokine production differed significantly from that in the corresponding cultures incubated without the presence of exogenic cytokines (*p < 0.05; **p < 0.01; ***p < 0.001). Lines over bars in A and B indicate the Mbv isolates for Tozasertib which the induced cytokine or NO production differed significantly STK38 from that induced by H37Rv (#p < 0.01; ##p < 0.001). To verify whether signaling pathways leading to NO production were differentially modulated by the mycobacterial strains, we evaluated induction of iNOS, the essential enzyme for the conversion of arginine to citrulline and NO. The results obtained showed that treatment with IFN-γ induced iNOS expression in the cultured macrophages, and subsequent infection of these cells with bacteria enhanced the level

of enzyme expression in a similar manner (Figure 4D), demonstrating no strain-specific difference in the regulation of IFN-γ-dependent signaling which leads to transactivation of the iNOS gene. Evaluation of expression of M2 markers in the cells pretreated with IFN-γ demonstrated LB-100 research buy suppression of Arg-1 expression induced by the strains B2 and H37Rv, but not those infected with strain MP287/03 (Figure 4E). Expression of MR by MΦ was slightly inhibited in the cell cultures treated with IFN-γ, and further reduced after infection of these cells with the strains B2 or H37Rv. In contrast, infection with the strain MP287/03 restored a high level of expression of this receptor (Figure 4E), suggesting induction of MR gene transcription due to mycobacteria in these cells.

6 -0.6 LSA1610 lsa1610 Hypothetical integral membrane protein -0.7   -0.9 LSA1617 lsa1617 Hypothetical protein     -0.7 LSA1620 lsa1620 Hypothetical protein     -0.6 LSA1623 lsa1623 Hypothetical integral membrane protein -0.5   -0.6 LSA1637 lsa1637 Hypothetical integral membrane protein, TerC family -1.7 -1.0 -1.6 LSA1644 lsa1644 Hypothetical protein 1.7   D LSA1649 selleck inhibitor lsa1649 Hypothetical extracellular protein precursor     -0.5 LSA1659 lsa1659 Hypothetical protein -0.5     LSA1662 lsa1662 Hypothetical protein -1.0 -0.6 -0.7 LSA1663 lsa1663 Hypothetical

protein -0.8     LSA1678 lsa1678 Hypothetical protein -0.6     LSA1680 lsa1680 Hypothetical protein -0.6     LSA1716 lsa1716 Hypothetical protein   -0.5   PRN1371 cost lsa1822 lsa1822 Hypothetical protein     -0.5 LSA1828 lsa1828 Hypothetical integral membrane protein 0.6 0.7   LSA1850 lsa1850 Hypothetical protein   -0.6   LSA1876 lsa1876 Hypothetical integral membrane protein     -0.6 LSA1877 lsa1877 Hypothetical protein     -0.6 Proteins of unknown function only similar to other proteins from the same organism LSA1159 lsa1159 Hypothetical cell surface protein precursor 2.0   0.5 LSA1165 lsa1165 Hypothetical cell surface protein precursor 1.8     LSA1700 lsa1700 Hypothetical protein 2.1 0.8   LSA1814 lsa1814 Hypothetical protein     -0.5 Proteins of unknown function. without

TGF-beta inhibitor similarity to other proteins LSA0065 lsa0065 Hypothetical integral membrane protein -0.5     LSA0093 lsa0093 Hypothetical integral membrane protein -0.9   -1.2 LSA0121

lsa0121 Hypothetical small peptide -0.7 -0.6 -0.5 LSA0163 lsa0163 Hypothetical protein   -1.1 -1.3 LSA0167 lsa0167 Hypothetical protein     -1.4 LSA0168 lsa0168 Hypothetical protein     -1.4 LSA0188 lsa0188 Hypothetical small peptide     -0.8 LSA0256_a lsa0256_a Hypothetical protein 2.3 1.0 2.2 LSA0257 lsa0257 Hypothetical protein 1.4     LSA0281 lsa0281 Hypothetical lipoprotein precursor   -0.5 -0.6 LSA0301 lsa0301 Hypothetical protein     0.6 LSA0334 lsa0334 Hypothetical extracellular protein precursor 1.1     LSA0339 lsa0339 Hypothetical protein -0.5     LSA0378 lsa0378 Hypothetical protein -0.7     LSA0514 lsa0514 Hypothetical small extracellular protein precursor   -0.8   LSA0534 lsa0534 Hypothetical cell surface protein precursor (with LPQTG sorting signal) Staurosporine nmr 1.0   D LSA0576 lsa0576 Hypothetical protein 0.5 D   LSA0641 lsa0641 Hypothetical extracellular peptide precursor   -0.5   LSA0647 lsa0647 Hypothetical extracellular protein precursor 0.6     LSA0667 lsa0667 Hypothetical protein 1.0   0.9 LSA0753 lsa0753 Hypothetical integral membrane protein     0.5 LSA0789 lsa0789 Hypothetical protein -1.9     LSA0837 lsa0837 Hypothetical protein 1.2 1.3 1.4 LSA0885 lsa0885 Hypothetical protein 1.8     LSA0902 lsa0902 Hypothetical protein 0.7 D   LSA0945 lsa0945 Hypothetical protein     0.9 LSA1019 lsa1019 Hypothetical cell surface protein precursor     0.8 LSA1035 lsa1035 Hypothetical small integral membrane protein     0.

Biochemical and

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In recent years, as a representative of new engineering materials, carbon nanotube (CNT) at nanoscale has shown superior mechanical, electrical, and thermal properties,

as well as low density and high aspect ratio, which make it an ideal choice for composite reinforcement. CNT-reinforced nanocomposite is a multi-phase material, and its external macro-physical Selleck PF-6463922 properties strongly depend on the properties of its constituents and complex internal microstructure. Experimental evaluation requires large amounts of material samples and a large testing work load, giving simulation of the physical properties of nanocomposites important engineering significance. There has been extensive research on the mechanical, Wortmannin in vitro thermal, and electrical properties of CNT-reinforced nanocomposites. For instance, the thermal properties [1–3] and electrical properties of CNT-reinforced nanocomposites [4, 5] have been explored experimentally in some previous studies. Moreover, due to the complexity and variations of the CNT-reinforced composite microstructure, theoretical analyses and numerical simulation methods are common strategies to estimate composite physical properties. For instance, diffusion and thermal expansion coefficients of CNT-reinforced nanocomposites have been studied through micromechanics models without sufficient atomic scale information [6] or molecular dynamics (MD)

models else with very high computational cost and complexity [7]. In recent years, to deal with the remarkable scale difference in CNT-reinforced

JSH-23 chemical structure nanocomposites, multi-scale modeling has been widely used for predicting the mechanical properties [8], electrical properties [9], and thermal conductivity [10] of the CNT-reinforced nanocomposites. However, to the best knowledge of the present authors, there has been no report on the multi-scale modeling of thermal expansion properties of the CNT-reinforced nanocomposites to date. In this work, the thermal expansion properties of the CNT-reinforced nanocomposites, i.e., CNT/epoxy, were evaluated using a sequential multi-scale numerical model. The present study focused on the effects of two key parameters, i.e., temperature and CNT content, on the thermal expansion properties. Moreover, it was found that the results of the present multi-scale numerical model agree very well with those based on theoretical predictions and experimental measurements carried out in this work. Methods To investigate the thermal expansion properties of CNT-reinforced nanocomposites, numerical simulations based on a sequential multi-scale approach were conducted on two types of microstructural models, a uni-directional model in which CNTs were uni-directionally aligned within epoxy and a multi-directional model in which the CNTs were randomly oriented within the epoxy.