03 (0) 13.3 (4.6)/0.25 (0) 8 (0)/0.16 (.08) 13.3 (4.6)/0.042 (.014) 16 (0)/4 (0) 6.6 (2.3)/6.6 (2.3) 8 (0)/0.16 (.08) 8 (0)/067 (.29) 2.6 (1.1)/0.42 (.14) 8 (0)/0.5 (0) 6.6 (2.3)/2 (0) 6.6 (2.3)/0.16 (0) 8 (0)/0.16 (.08) Tetracycline Determination of the chemosusceptibility of H. pylori strains

to polysorbate 80 used in association with clarithromycin or metronidazole The combination of polysorbate 80 with metronidazole increased the size of the growth inhibition halos (Figure 1); around the disk Selleck ABT263 containing polysorbate 80, a minimal halo of complete inhibition of growth, ~1 mm, can be seen. Subculture tests showed the presence of another halo of about 4 mm contains developed dead bacteria. Selleckchem LCL161 The same effect was observed when clarithromycin was assayed alone and with polysorbate 80 (data not shown). Halo sizes around discs charged with polysorbate 80 and amoxicillin, or levofloxacin, or tetracycline were not larger than those obtained with single antibiotics (data not shown). The synergistic effect of the association polysorbate 80/clarithromycin and polysorbate 80/metronidazole was confirmed by

the broth dilution Dipeptidyl peptidase tests (Table 2). When used in association, the MBCs of polysorbate 80 decreased by 2–4 times and those of antibiotics by 2–16 times, compared to the respective MBCs of drugs used alone. The effect of the association of polysorbate 80 with amoxicillin, or levofloxacin, or tetracycline was negligible (Table 2). Figure 1 The combination of polysorbate 80 with metronidazole (disc on the right) increases the size of the growth inhibition halo; the disc on the left was charged with metronidazole

alone and the disc at the top with polysorbate 80 alone. TEM analysis of CCUG 17874 and C/M-R2 H. pylori strains treated with polysorbate 80, alone and in association with clarithromycin and metronidazole The ultrastructural click here characteristics of the two untreated strains appeared different from each other. CCUG 17874 H. pylori organisms showed homogeneous cytoplasm and rare detachment membrane/cytoplasm (Table 3, Figure 2A); ~ 5% of cells presented an altered profile. C/M-R2 organisms showed homogeneous cytoplasm and vesicles (Figure 2B). In both strains, flagella have been observed (Table 3). Table 3 Approximate percentages of organisms showing ultrastructural alterations observed in two H.

Furthermore, the anti-angiogenic activity of platycodin D was

confirmed by performing the Matrigel plug assay in mice. In a mouse tumor xenograft model, platycodin D inhibited the growth of MDA-MB-231 breast carcinoma, and reduced the expression of VEGF, CD34 and IL-8. Taken together, our results indicate that platycodin SB431542 chemical structure D exerts anti-angiogenic action by regulating MAPKs activation and IL-8 expression. Therefore, platycodin D may beneficial for prevention and treatment of angiogenesis-dependent human diseases such as tumor. Poster No. 85 Role of Complement in Lymphoid-Like Tumor Transformation and Invasion Iraklis C. Kourtis 1 , Jacqueline D. Shields1, Melody A. Swartz1 1 Institute of Bioengineering, Ecole Polytechnique Fédérale de Lausanne, Lausanne, Vaud, Switzerland Changes in the immunological equilibrium in the tumor microenvironment are critical for the progression of a developing tumor, allowing tumor escape from immune surveillance and metastases. We have identified that invasive B16 F10 melanomas

naturally secrete CCL21, a ligand for CCR7, which is used by dendritic cells and naïve T cells to home to the T cell zone of the lymph node to initiate an immune response. B16 F10 melanoma cells were engineered to either knockdown, maintain or over-express CCL21. Chemokine secreting tumors, but not knockdown variants, SB202190 cost attracted CCR7+ lymphoid tissue inducer cells (LTis, CD45+CD3−CD4+IL-7Ra+ROR-γt+) into the tumor and drove lymphoid-like changes in the tumor click here microenvironment including a reticular fibroblast stromal network (CCL21+gp38+ ERTR7+LYVE-1−) surrounding the tumor, HEV-like vessels (ERTR7+ PNAds+LYVE-1−) inside the tumor, and, importantly, an overexpression of complement regulating receptors. This microenvironment, reminiscent of the T cell zone in the lymph node, attracted naive T cells into the tumor where, we hypothesized, they could be educated towards a tolerogenic phenotype only in a regulatory

microenvironment. Recent studies have suggested a role of complement in tumor growth, and since complement can serve both immune regulatory and functional roles depending its processed form, we implanted of these tumors into C3-/- mice. We found that both CCL21 expressing and knockdown tumors grew poorly, and CCL21-secreting tumors could not drive a regulatory T cell response as they did in wild type mice. These findings suggest that invasive tumors may utilize complement dependent strategies in the newly formed quasi lymph node microenvironment, to further provide a regulatory environment for in situ education of T cells shifting the host immune response from a functional to regulatory repertoire. Poster No.

astaci (Saprolegniales, Oomycetes). Crayfish plague-associated die-offs in Austrian waters were first reported in 1879 [9] and in the 1920s [10], and continue sporadically into the present. An estimated 80% of all native Austrian crayfish populations disappeared in the 20th century (Pöckl, personal communication). A high HMPL-504 mw percentage of these die-offs are associated with crayfish plague, which represents one of the major threats to the recovery of populations of native crayfish species in

Central Europe [11]. For example, Astacus astacus, formerly a very abundant species in Europe, is now considered threatened by the International Union for Conservation of Nature and Natural Resources (IUCN) [12]. In many countries this economically find more valuable crayfish is on the Red List and its current harvest is probably less than 10% of the harvest

rate before introduction of the crayfish-plague pathogen [13, 14]. A. astaci was introduced from North America, where various species harbour the pathogen without showing clinical signs of infection. Crayfish-plague outbreaks among such populations often occur only under stress conditions. The introduction of resistant North American species like the signal crayfish (Pacifastacus leniusculus), the red-swamp crayfish (Procambarus clarkii) and the spiny-cheek crayfish (Orconectes limosus) http://​www.​issg.​org/​database MM-102 supplier has established a permanent reservoir for the pest in Europe. The transmission of the pathogen occurs via crayfish cadavers, crayfish-feeding fish [15], Thiamet G fish scales [16] and all kinds of equipment, which have been in contact with contaminated water [10].

The adaptive life style, high fecundity, and resistance to the pathogen make introduced crayfish species a potent bioinvador and the most dangerous vector for pathogen transmission. Biflagellated secondary zoospores, measuring 8 × 12 μm, represent the infective unit of A. astaci. They target host tissue by various mechanisms including chemotaxis [17, 18] on soft parts of the crayfish integument, especially at the joints, the bottom side of the abdomen and even near the eyestalks [19] as well as fresh wounds [20]. Once zoospores reach the upper lipoprotein-layer of the crayfish cuticle, they discard their flagellae, and develop a penetration peg, that weakens the lipid layer enzymatically [21]. Soon after the germ tube has penetrated the cuticle by mechanical force, the developing hyphae begin to secrete chitinases and proteases [22]. In this phase different chitinases [18] jointly degrade chitin polymers in order to release nutrients and facilitate further growth mainly parallel to the chitin fibrils of the endocuticula [23].

2000). Furthermore, low Taxol concentrations, comparable to the levels we detected in endophyte extracts, did not affect the physiological properties of the membrane (Balasubramanian and Straubinger 1994; Sharma and Straubinger 1994; Bernsdorf et al. 1999; Crosasso et al. 2000; Zhao and Feng 2004). Although these experiments involved artificial membranes, there is also evidence

that fungi can take up non-polar compounds by passive transport and store them in vesicles. For example, Fusarium solani can absorb polyaromatic compounds from the cell culture medium and store them within intracellular compartments with no impact on growth (Verdin et al. 2005). In the endophytes we studied, the accumulation of non-polar taxoid molecules in lipophilic cell structures combined with the high sensitivity of our analytical methods, immunological detection and LC/MS/MS-based multi-reaction monitoring (MRM) ensured that these PI3K Inhibitor Library carry-overs could be detected. After the first and second passages of the fungal cultures, no taxanes could be detected by LC/MS/MS. The fungi were no longer associated with the Taxol source and 4EGI-1 in vitro hence the trace amounts of taxanes detected initially were diluted below the detection limit. Our

results and conclusions therefore offer a satisfactory explanation for the contradictory results in earlier publications, some providing evidence for independent taxane biosynthesis in different endophytic fungi and others lacking this evidence. Acknowledgments U.H. was supported by a pre-doctoral fellowship from the Volkswagen Foundation, Hannover, Germany (AZ.: I/82 754). Open Access This article is distributed under the terms of the Creative Commons Attribution License which permits any use, distribution, and reproduction in any medium, provided the original author(s) and the source

are credited. Electronic supplementary material Below is the link to the electronic supplementary material. ESM 1 (DOCX 666 kb) References Agger S, Lopez-Gallego F, Schmidt-Dannert C (2009) Diversity of sesquiterpene synthases in the basidiomycete Coprinus cinereus. Mol Microbiol 72(5):1181–1195PubMedCrossRef Balasubramanian SV, Straubinger RM (1994) Taxol–lipid interactions: taxol-dependent effects on the physical properties of model membranes. Biochemistry Gemcitabine 33:8941–8947PubMedCrossRef Baloglu E, Kingston DGI (1999) Taxane diterpenoids. J Nat Prod 62:1448–1472PubMedCrossRef Bernsdorf C, Reszka R, Winter R (1999) Interaction of the anticancer agent Taxol (paclitaxel) with phospholipid bilayers. J Biomed Mater Res 46:141–149CrossRef Bömke C, Tudzynski B (2009) Diversity, regulation, and evolution of the gibberellin biosynthetic pathway in fungi compared to plants and bacteria. Phytochemistry 70:1876–Ilomastat order 1893PubMedCrossRef Brown DT (2003) Preclinical and clinical studies of the taxanes. In: Itokawa H, Lee K-H (eds) The genus Taxus.

Three genes or operons, namely znuA, znuCB and ykgM were further identified as direct Zur targets. Subsequent determination of transcription start sites, predicted -10/-35 elements, and Zur binding sites enabled the mapping of Zur-DNA interactions for these three genes. This study confirmed that Y. pestis Zur employed a conserved regulatory mechanism observed in γ-Proteobacteria. Methods Bacterial strains The wild-type (WT) Y. pestis biovar Microtus strain 201 is avirulent to humans but highly lethal to mice [12]. It was grown in Luria-Bertani (LB) broth or chemically

defined TMH medium [13] at 26 or 37°C. E. coli strains BL21 (DE3) was grown in LB broth at 37°C. Antibiotics were added at the following concentrations when required: 100 μg/ml for ampicillin, and 50 μg/ml for kanamycin. Construction of the zur Selleck Tideglusib mutant BTK inhibitor The Y. pestis zur mutant strain (Δzur) was generated by using the one-step inactivation method based on the lambda phage recombination system, as previously described by Datsenko and Wanner [14]. Briefly, the helper plasmid pKD46 was first transformed into Y. pestis 201. The zur::kana mutagenic cassette was PCR

amplified from plasmid pRS551 [15] with the primers zur-k-F and zur-k-R and transformed into strain 201/pKD46 (all the primers used in this study were listed in Additional file 1). Mutants were selected by plating electroporated cells on agar plates containing kanamycin. Colonies of resistant transformants were subsequently selected. Chromosomal integration of the mutagenic cassette was confirmed by PCR and 6-phosphogluconolactonase sequencing using SB202190 cost oligonucleotides external to the integrated cassette (data not shown). The mutants were incubated overnight at 37°C and then tested for the loss of the temperature-sensitive plasmid pKD46 by looking for ampicillin sensitivity. The elimination of the helper plasmid was verified by PCR (data not shown). Bacterial growth and RNA isolation A chemically defined TMH medium [13] was used to cultivate strain 201. Both WT and Δzur were pre-cultivated at

26°C to the middle exponential growth phase (OD620 about 1.0) in TMH medium. The cell cultures were then diluted 1:20 in fresh TMH medium and grown at 26°C until an OD620 of about 1.0. Finally, 5 mM ZnCl2 was added into each cell culture to ensure zinc rich conditions. Growth was continued for 30 min at 26°C before harvested for total RNA isolation. This kind of treatment with Zn had no toxic effect on both WT and Δzur, according to the colony counting assay (Additional file 1). Immediately before being harvested, bacterial cultures were mixed with two fold of RNAprotect Bacteria Reagent (Qiagen) to minimize RNA degradation. Total cellular RNA was isolated using the MasterPure™ RNA Purification kits (Epicenter). RNA quality was monitored by agarose gel electrophoresis and RNA quantity was measured by spectrophotometer.

oneidensis to form pellicles in the presence of EDTA completely. In contrast, Mg(II) shows mild effects on relieving EDTA inhibition whereas Fe(II) and Fe(III) counteracted EDTA in a way different from other tested cations evidenced by the fragile pellicles. In combination, these

data suggest that the relative stability constants of metal cations (Cu(II) [5.77], Mg(II) [8.83], Ca(II) [10.61], Mn(II) [15.6], Zn(II) [17.5], Fe(II) [25.0], and Fe(III) [27.2]) and their affect on EDTA inhibition are not correlated. It is particularly worth discussing roles of Fe(II) and Fe(III) in pellicle formation of S. oneidensis. In recent years, many INCB28060 in vitro reports have demonstrated that the iron cations are important, if not essential, in bacterial biofilm formation [34, 45–47]. In P. aeruginosa, influence of Fe(II) and Fe(III) on the process was equivalent to that of Ca(II) [34]. In S. oneidensis, irons in forms of Fe(II) and Fe(III) were Semaxanib mouse not only unable to neutralize selleck chemicals the inhibitory effect of EDTA on pellicle formation

completely but also resulted in structurally impaired pellicles although these agents indeed play a role in pellicle formation. This observation indicates that irons are not so crucial as Cu(II), Ca(II), Mn(II), and Zn(II) in pellicle formation of S. oneidensis. In fact, this may not be surprising. In Acinetobacter baumannii and Staphylococcus aureus, iron limitation improved biofilm formation

[48, 49]. Therefore, it is possible that different bacteria respond to irons in a different way with respect to biofilm formation. Like SSA biofilms, pellicles require EPS to form a matrix to support embedded cells. Although EPS are now widely recognized as the essential components for biofilm formation and development in all biofilm-forming microorganisms studied so far, diversity in their individual composition and relative abundance of certain elements is substantial [50]. For example, extracellular nucleic acids, which are not important in most biofilm-forming microorganisms, are required for SSA biofilm formation in a variety HSP90 of bacteria [11, 36, 37, 51, 52]. In S. oneidensis, proteins not extracellular DNAs are required to pellicle formation. While essential extracellular proteins for S. oneidensis pellicle formation are largely unknown, results from this study demonstrated that the AggA TISS is crucial in the process, likely at the development of the monolayer. One of substrates of this transporter is predicted to be SO4317, a large ‘putative RTX toxin’ [35], implicating that the protein may be involved in pellicle formation. In the case of polysaccharides, mannose dominates not only in pellicles but also in supernatants, implicating that mannose-based polysaccharides may have a more general role in the bacterial physiology. Like in B. subtilis, mutations in S.

Among peaks assigned to PANI, the characteristic peaks around 1,580 and 1,497 cm−1 relate to the stretching vibration of quinoid (−N=(C6H4)=N-) ring and benzenoid (−(C6H4)-) ring, respectively. Another main band at 1,303 cm−1 can be assigned to the stretching of C-N in -NH-(C6H4)-NH-. The bands selleck chemicals appeared at 1,143 cm−1 and 829 cm−1 which correspond to the stretching of C-H in-plane and C-H out-of-plane bendings. In addition, the bands of N-H (PANI) and O-H (H2O) at 3,230 and 3,400 cm−1, respectively, are observed. As noticed, the band near 3,400 cm−1

(O-H) is becoming intense with the decrease of the acid concentration, which is attributed to the appearance of hydrate MnO2. The above conclusion is proved by the annealing experiments: the band at 3,400 cm−1 (O-H) of hydrate MnO2 vanished after 500°C heat treatment (Additional file 1: Figure S1). The band PF01367338 near 1,303 cm−1 is becoming weaker from curves g to a in Figure 4, which MK-1775 price suggests that the doping degree of PANI is changing with the acid concentration. The characteristic bands of curves a, b, and c in Figure 4 shifted right compared with the others, which is ascribed to the effect of MnO2 on PANI. It demonstrates that some special interaction exists between MnO2 and PANI. Figure 4 FTIR spectra of the as-prepared samples. Curves a to g: MnO2/PANI fabricated in 0, 0.02, 0.05, 0.1, 0.2, 0.5, and 1 M HClO4, respectively.

Due to the ordered and metallic-like property, conducting polymers possess particular crystallinity and orientation. As shown in the XRD patterns in Figure 5A, there are no identified peaks appeared for the products synthesized in low-acid concentrations (curves a to e: 0.1 M NaOH, and 0, 0.02, 0.05, and 0.1 M HClO4, respectively), which indicates the products are amorphous. For the products obtained at 0.2 (curve f), 0.5 (curve g), and 1 M HClO4 (curve h), two intense XRD peaks 2θ≈20 and 25° are observed corresponding

to pure PANI according to previous literature [2]. All above results confirm that the crystallized PANI can be formed at higher acid concentrations in this work. Figure 5 XRD patterns of the samples. (A) The XRD patterns of the composites, curves a to h: MnO2/PANI fabricated in 0.1 M NaOH and 0, 0.02, 0.05, 0.1, 0.2, 0.5, and 1 M HClO4, respectively. (B) N-acetylglucosamine-1-phosphate transferase XRD pattern of the samples, curves a to d: annealed MnO2/PANI fabricated in 0, 0.02, 0.05, and 0.1 M HClO4, respectively. To further analyze the components at different acid concentrations, the samples were treated at 500°C (at which MnOx is crystallizing and PANI will be burned). The products obtained at 1, 0.5, and 0.2 M HClO4 were burned out with no solids left, which indicates that there is no MnO2 generating at such acid concentrations. Contrary to higher acid concentration, the solid residue of the products obtained at 0.1, 0.05, 0.02, and 0 M HClO4 turned black.

03); **represents significant difference between

group ’1%FBS + 10 ng/ml TGF-β1′ and group ’1%FBS’ (P = 0.044). Figure 6 The effects of TGF-β1 on expression levels of PKCα and p38 MAPK. BxPC3 cells were treated with 0.1, 1 and 10 ng/ml TGF-β1 for 10 min, 30 min and 24 h. Total cellular protein was extracted and subjected to western blotting analysis to detect expression of PKCα, phosphorylated-p38/total p38 MAPK and phosphorylated-ERK1/2/total ERK1/2. Bx represents BxPC3 cells and Bx/T represents the stably transfected BxPC3 cells with TGF-β1 plasmid. To determine whether the induced PKCα activity is responsible for the TGF-β1-induced decrease in the sensitivity of BxPC3 cells to cisplatin, we treated the cells with a selective PKCα inhibitor, Gö6976, and assessed TGF-β1-induced drug resistance. We found that inhibition of PKCα

activity could partially reverse TGF-β1-induced drug resistance of BxPC3 cells to 3-Methyladenine mouse cisplatin click here (Figure 7). Figure 7 MTT assay. (A) BxPC3 cells were grown in DMEM containing 5 μg/ml of TGF-β1 and then treated with or without Gö6976, an inhibitor of PKCα at the indicated concentrations. After this pretreatment, the cells were further treated with cisplatin for an additional 48 h, and the cell viability was determined via MTT assay. (B) IC50 values. * represents a significant difference in IC50 values between groups for TGF-β1 (5 ng/ml) and all other groups. selleck inhibitor Blockade of PKCα and TβRII reversed mafosfamide the resistant status of BxPC3 cells We designed and constructed a TGF-β type II receptor (TβRII) siRNA expression vector to knockdown TβRII expression. We stably transfected the TβRII siRNA vector into BxPC3 cells and isolated three stable clones.

Western blotting analysis showed that TβRII expression was significantly knocked down in clone 2 relative to the other two clones (Figure 8A). We chose clone 2 for the following experiments. The IC50 of clone 2 to gemcitabine was 812 μg/ml, much lower than that for the vector-only-transfected BxPC3 and the parental cells (Figure 8B), indicating that knockdown of TβRII increases the mortality of cancer cells and increases sensitivity to gemcitabine. Figure 8 Role of TβRII siRNA in BxPC3 cells. (A) Western blotting analysis of TβRII (type II receptor or TGF-β1) protein levels. BxPC3 cells were grown and transfected with TβRII siRNA. After selection with G418, three clones were isolated and the cells from these clones underwent protein isolation. They were subjected to Western blotting analysis with anti-TβRII antibody. Lane 1, total pool of BxPC3 cells; lane 2, mock clone (transfected with empty plasmid, psilenser 2.1 U6); lane 3, knockdown (KD) clone 1; lane 4, KD clone 2; and lane 5, KD clone 3. (B) MTT assay. The transfected BxPC3 cells were grown and treated with gemcitabine at the indicated doses for 2 days. The cell viability was detected by using the MTT assay.

Human bone metastatic prostate cancer C4-2B cells were also co-cultured with

human microvessel cells. All cultures were performed in triplicate. When the cells reached 90% confluence on the third day after they were seeded, the media were changed to complete learn more culture media with 25 or 250 μg/mL bevacizumab, or an equal amount of IgG1. The cell culture media were collected at 72 hours after treatment in culture medium with 2% FBS in 5% CO2 at 37°C. The levels of VEGF, Epacadostat clinical trial bFGF and IL-8 in the supernatants were measured with an ELISA kit (Quantikine; R&D Systems, Minneapolis,MN) according to the manufacturer’s instructions. Cell proliferation assay A density of 5×103 cells per well was seeded on 96-well-plate

overnight in complete culture medium and then treated with bevacizumab or control IgG or recombinant human VEGF in complete culture medium without fetal bovine serum for a 3-day incubation. The cell numbers were measured every 24 hours by mitochondrial 3-(4,5-dimethylthiazol-2-yl)-5-(3-carboxymethoxyphenyl)-2-(4-sulfophenyl)-2 H-tetrazolium, inner salt (MTS) assay with use of the CellTiter 96 Aqueous One Solution Cell Proliferation Assay (Promega) according to the manufacturer’s instructions. Invasion assay When C4-2B cells reached below 80% confluence, serum containing medium was removed and replaced with serum-free medium containing bevacizumab (100 μg/mL) ACP-196 order or an equal amount of IgG, and cultures were returned to an incubator for 24 hours. The in vitro invasion assay was performed with a 24-well collagen-based cell invasion assay

kit (Millipore). 2 × 105 of C4-2B cells in 300 μl culture medium containing also 100 μg/ml bevacizumab or IgG were placed into an invasion chamber consisting of a 24-well collagen-based plate. In order to observe the direct role of VEGF on the invasion of C4-2B cells, recombinant human VEGF (100 ng/ml) was added to the lower chamber. The cells were incubated for 24 h at 37°C in a 5% CO2 incubator. The non-invading cells in the media were discarded from the top of the insert. The invasive cells on the lower surface of the membrane were stained by the green fluorescent dye Calcein AM (Invitrogen) in PBS at 37°C for 1 h. The fluorescently labeled cells were photographed under a fluorescence microscope. The fluorescence of the invaded cells was read by a microplate reader at excitation/emission wavelength of 530/590 nm. In vitro angiogenesis assay When C4-2B cells reach 80% confluence, they were cultured in serum-free RPMI1640 treated with bevacizumab (100 μg/mL) or an equal amount of IgG for 24 h. The conditioned media were collected, centrifuged, and transferred to fresh tubes.

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BR, Soref RA, Del Alamo J: Carrier-induced change in refractive index of InP, GaAs, and InGaAsP. IEEE J Quantum Electron 1990,26(1): 113–122.CrossRef 46. Veselago VG: The electrodynamics of substances with simultaneously negative values of ϵ and μ . Physics-Uspekhi 1968, IMP dehydrogenase 10:509–514.CrossRef 47. Yu ZG, Krishnamurthy S, Guha S: Photoexcited-carrier-induced refractive index change in small bandgap semiconductors. J Opt Soc Am B 2006,23(11): 2356–2360.CrossRef 48. Akhmanov A, Nikitin SY: Physical Optics. Oxford: Oxford University Press; 1997. Competing interests The authors declare that they have no competing interests. Authors’ contributions VM designed and performed the optical experiments (z-scan and spectroscopy), participated in the analysis and interpretation of data, and prepared the draft and final version of the manuscript. AN, VV, and VS designed and performed the chemical experiments, achieved that nanoparticle was covered with a monolayer of oleic acid, prepared the sections ‘Synthesis of nanoparticle’ and ‘Composite preparation’. YK and VD conceived of the study, participated in the analysis and interpretation of data, helped to draft the final version of the manuscript.