Sierra Leone J Biomed Res 2012,4(1): 43–52.

45. Aires de Sousa M, Conceicao T, de Lancastre H: Unusually high prevalence of nosocomial Panton-Valentine leukocidin –positive Staphylococcus aureus isolates in Cape Verdes Island. J Clin Microbiol 2006, 44:37–3793. 46. Campbell SJ, Deshmukl HS, Nelson CL, Bae I: Genotypic characterization of Staphylococcus aureus isolates from a multinational trial of topical drugs for skin and skin stricture infections. J Clin Microbiol 2008, 46:678–684.PubMedCrossRef 47. Goering RV, Shawar RM, Scangarella NE, OHara FP, Amrine-Madsen H, West JM, Dalessandro M, Becker JA, Walsh SL, Miller LA, van Horn SF, Thomas ES, Twynholm T: Molecular epidemiology of methicillin-resistant and methicillin-susceptible Staphylococcus aureus isolates from global Dabrafenib supplier clinical trial. J Clin Microbiol 2008, 9:2842–2847.CrossRef 48. Prévost G, Mourey L, Colin DA, Menestrina G: Staphylococcal pore-forming toxins. Curr Top Microbiol Immunol 2001, 257:53–83.PubMedCrossRef 49. Genestier AL, Michallet MC, Prevost G, Bellot G, Chalabreysse L, Peyrol S, Thivolet F, Etienne J, Lina G, Vallette FM, Vandenesch www.selleckchem.com/products/PD-0332991.html F, Genestier L: Staphylococcus aureus Panton-Valentine leukocidin directly targets mitochondria and induces Bax-independent apoptosis of human neutrophils. J Clin Invest 2005, 115:3117–3127.PubMedCrossRef 50. Ladhani S: Understanding the

mechanism of action of the exfoliative toxins of Staphylococcus aureus . FEMS Immunol Med Microbiol 2003, 39:181–189.PubMedCrossRef

51. Prevost G, Couppie P, Monteil H: Staphylococcal epidermolysins. Curr Opin Infect Dis. 2003, 16:71–76.CrossRef 52. Vandenesch F, Naimi T, Enright MC, Lina G, Nimmo GR, Heffernan H, Liassine N, Bes M, Greenland T, Reverdy ME, Etienne J: Community acquired methicillin-resistant Staphylococcus aureus carrying Panton-Valentine leukocidin genes: worldwide emergence. Emerg Infect Dis 2003, 9:978–984.PubMedCrossRef 53. Morris CA, Conway HD, Everall PH: Food-poisoning due to staphylococcal enterotoxin E. Lancet 1972, 2:1375–1376.PubMedCrossRef 54. Chen TR, Chiou CS, Tsen HY: Use of Novel PCR Primers Specific to the Genes of Staphylococcal Enterotoxin G, H, I for the Survey of Staphylococcus aureus Strains Isolated From Food-Poisoning Cases and Food Samples in Taiwan. PD-1 inhibitor Int J Food Microbiol 2004, 92:189–197.PubMedCrossRef 55. Ikeda T, Tamate N, Yamaguchi K, Makino S: Mass Outbreak of Food Poisoning Disease Caused by Small Amounts of Staphylococcal Enterotoxins A and H. Appl Environ Microbiol 2005, 71:2793–2795.PubMedCrossRef 56. Daum RS, Ito T, Hiramatsu K, Hussain F, Mongkolrattanothai K, Jamklang M, Boyle-Vavra S: A novel methicillin-resistance cassette in community-acquired methicillin-resistant Staphylococcus aureus isolates of diverse genetic backgrounds. J Infect Dis 2002, 186:1344–1347.PubMedCrossRef 57.

Staining intensity was not graded to avoid subjective interpretation. Scoring of the Akt immunostaining Cases were considered positive for p-Akt and Akt2 when cytoplasmic as well as nuclear staining was strong and clearly different from that of the surrounding normal epithelium, independently of the number of positive cells [24]. Staining intensity was not graded to avoid subjective interpretation. Results and discussion HPV DNA in different specimens Thirty-seven immunocompetent patients referred to the Dermatology Clinic at San Gallicano Institute and affected by BCC were included in the study. The mean age was 62 ± 15 years. Data for each patient are reported in Table 1. Ten and

fifteen BCC were from the trunk and back respectively, 7 from the extremities and 5 from the head and neck region. Neratinib supplier Each bioptic skin sample underwent to immunohistochemical analysis and HPV nested PCR on consecutive slices. In all samples the HPV DNA was detected in 26 of 37 (70,3%) lesional skins and in 19 of 37 (51,3%) perilesional areas. No alfa or gamma papillomavirus was detected. Forehead swabs showed positivity

for beta-HPV in 34 of 37 (91,9%) samples. Gefitinib research buy Similar proportions of HPV positive forehead samples were already described in individuals with skin cancer [25, 26]. No statistically significant association was revealed among HPV presence, phototype, or anatomical localization. Among the detected papillomaviruses in all analyzed samples, HPV38 was the most frequent type (Figure 1). Figure 1 HPV typing. HPV types were detected as in Methods and are reported as number of positive samples for each type in all analysed specimens. In the HPV DNA-positive BCC

samples, 16 different types of beta-HPV were found and the most frequent types were HPV107 (15,4%), HPV100 (11,5%) and HPV15 (11,5%) all belonging to the β-HPV species 2, while in perilesional samples the different HPV types detected were 9 and the most frequent was the HPV38 (26,3%) (Figure 2). Forslund et al [27] found that in sun-exposed skin, cutaneous species 2 HPVs were predominating in SCC. Although the number of specimens analyzed in this study is not suitable to state the prevalence rate of HPV species, our RANTES data can lead to hypothesize a correlation between beta-HPV species 2 and BCC. However some serological studies showed no firm association of both cutaneous and genital HPV with BCC [28, 29]. Figure 2 HPV types in BCC and normal samples. The HPV types are reported as percentage of positive samples in basal cell carcinoma (BCC), normal skin and forehead swabs. The HPV types found in forehead swabs were 18 and the most frequent type was HPV100 (17,6%). No correspondence of HPV type between BCC and swab samples was found, whereas a correspondence between perilesional normal skin and BCC was found in three samples (Table 1). Rollison et al.

aureus under the impact of antibiotics administered for chemotherapy. J Clin Microbiol 2003, 41:1687–1693.PubMedCrossRef 45. McAleese F, Wu SW, Sieradzki K, Dunman P, Murphy E, Projan S: Overexpression of genes of the cell wall stimulon in clinical isolates of Staphylococcus aureus exhibiting vancomycin-intermediate- S. aureus -type resistance to vancomycin. J Bacteriol 2006, 188:1120–1133.PubMedCrossRef 46. Yang SJ, Dunman PM, Projan SJ, Bayles KW: Characterization of the Staphylococcus Cilomilast solubility dmso aureus CidR regulon: elucidation

of a novel role for acetoin metabolism in cell death and lysis. Mol Microbiol 2006, 60:458–468.PubMedCrossRef 47. Weinrick B, Dunman Pexidartinib nmr PM, McAleese F, Murphy E, Projan SJ, Fang Y: Effect of mild acid on gene expression in Staphylococcus aureus . J Bacteriol 2004, 186:8407–8423.PubMedCrossRef 48. Nelson JL, Rice KC, Slater SR, Fox PM, Archer GL, Bayles KW: Vancomycin-intermediate Staphylococcus aureus strains have impaired acetate catabolism: implications for polysaccharide intercellular adhesin synthesis and autolysis. Antimicrob Agents Chemother 2007, 51:616–622.PubMedCrossRef 49. Booth IR: Regulation of cytoplasmic

pH in bacteria. Microbiol Rev 1985, 49:359–378.PubMed 50. Schulthess B, Meier S, Homerova D, Goerke C, Wolz C, Kormanec J: Functional characterization of the sigmaB-dependent yabJ-spoVG operon in Staphylococcus aureus : role in methicillin and glycopeptide resistance.

Antimicrob Agents Chemother Fludarabine cost 2009, 53:1832–1839.PubMedCrossRef 51. Sau S, Bhasin N, Wann ER, Lee JC, Foster TJ, Lee CY: The Staphylococcus aureus allelic genetic loci for serotype 5 and 8 capsule expression contain the type-specific genes flanked by common genes. Microbiology 1997, 143:2395–2405.PubMedCrossRef 52. Luong T, Sau S, Gomez M, Lee JC, Lee CY: Regulation of Staphylococcus aureus capsular polysaccharide expression by agr and sarA . Infect Immun 2002, 70:444–450.PubMedCrossRef 53. O’Riordan K, Lee JC: Staphylococcus aureus capsular polysaccharides. Clin Microbiol Rev 2004, 17:218–234.PubMedCrossRef 54. Campos MA, Vargas MA, Regueiro V, Llompart CM, Alberti S, Bengoechea JA: Capsule polysaccharide mediates bacterial resistance to antimicrobial peptides. Infect Immun 2004, 72:7107–7114.PubMedCrossRef 55. Llobet E, Tomas JM, Bengoechea JA: Capsule polysaccharide is a bacterial decoy for antimicrobial peptides. Microbiology 2008, 154:3877–3886.PubMedCrossRef 56. Boyle-Vavra S, Berke SK, Lee JC, Daum RS: Reversion of the glycopeptide resistance phenotype in Staphylococcus aureus clinical isolates. Antimicrob Agents Chemother 2000, 44:272–277.PubMedCrossRef 57.

1a, b), selleck compound establishing the diagnosis of

emphysematous pyelonephritis. Despite emergent radical nephrectomy with potent intravenous antibiotics, the patient expired due to septic shock 10 h postoperatively. Fig. 1 Transverse view (a) and coronal view (b) from contrast-enhanced computed tomography of a 56-year-old woman showing massive gas within (arrowheads) and around (arrows) the enlarged right kidney Emphysematous pyelonephritis, occurring with predisposing factors including diabetes and urinary tract obstruction, is potentially fatal. Early image interventions are warranted for those with toxic manifestations or prolonged fever of up to 10–14 days despite antibiotic treatment. Conflict of interest The authors have declared that no conflict of interest exists.”
“Guest Editors Kawahara K (Sagamihara), Kusano E (Shimotsuke), Mitarai T (Kawagoe), Tomita K (Kumamoto), and Uchida S (Tokyo) Special advisors Kimura G (Nagoya), Lang NSC 683864 concentration F (Tübingen), Palmer LG (New York) Schematic representation of claudin-based tight junctions in epithelia, from the paper by S. Muto et al. in this issue”
“Introduction Drug-related rash with eosinophilia and systemic symptoms (DRESS) or drug-induced hypersensitivity syndrome (DIHS) is a life-threatening

multiorgan systemic reaction characterized by rash, fever, lymphadenopathy, hepatitis, and leukocytosis with eosinophilia [1]. These conditions are caused by a limited number of drugs, including carbamazepine, phenytoin, phenobarbital, zonisamide, allopurinol, dapsone, salazosulfapyridine, and mexiletine [2]. Renal dysfunction associated with DIHS/DRESS has been reported to occur in 10% of cases and is attributable to acute interstitial nephritis (AIN) [2, 3]. In rare cases with DIHS, granuloma formation has also been described, i.e., granulomatous interstitial nephritis (GIN) [4–6]. Here we describe the case of a patient with

bipolar disorder and biopsy-proven GIN that developed during the course of carbamazepine-induced DIHS/DRESS. Case report A 70-year-old woman was admitted to our hospital because of high fever and acute kidney injury. She had been visiting a psychiatric clinic for bipolar disorder since the age of 48 years and another medical clinic for mild hypertension since the age of 63 years. She had no history of allergic Afatinib in vitro disorders or tuberculosis. Approximately 50 days before admission, she was switched from valproic acid to 200 mg/day carbamazepine (CBZ) for mood swings. Approximately 40 days after initiation of CBZ, she presented with purpura on the legs. She visited her regular physician. Laboratory analyses revealed platelets of 10.6 × 104/μL, aspartate aminotransferase (AST) of 62 IU/L, alanine aminotransferase (ALT) of 107 IU/L, C-reactive protein (CRP) of 2.65 mg/dL, and serum creatinine (sCr) of 0.76 mg/dL. Tranexamic acid (750 mg/day) and levofloxacin (LVFX, 300 mg/day) were prescribed.

Most probes used for the final array construction were oligonucleotide probes identified in public databases as the probe sequences were diverse and minimal cross-hybridization was obtained. Some sequence data is available upon request. Optimization of labeling and hybridization conditions To avoid amplification bias and to get a more uniform genetic locus representation, targets

were labeled using a random approach that does not involve amplification. All labeled target DNA positively hybridized to the array (Figure 1) showing fluorescent net signal intensities ranging from 2000 to 6000 intensity units demonstrating efficient hybridization of the target DNA. The hybridization conditions were further tested to get the optimal discrimination of target species and genes leading to toxin production without having unspecific signal intensities by determining the optimal PCR annealing temperature selleck screening library for fungal DNA using the probes in Table 1. Aspergillus clavatus and A. versicolor were used for this purpose as they showed cross-hybridization to other species-specific probes in the initial experiment. This was expected as the ITS region of both species are very similar. An increase in hybridization temperature from 42°C to 53°C showed that there is nearly no cross-hybridization between these two species and there was no decrease in net signal learn more intensity (results not shown). Although the ITS sequences

are quite similar for both fungal species, high hybridization efficiencies were obtained with net signal intensities of about 2000 signal units for A. clavatus and of about 3500 signal units for A. versicolor (Figure 2A). In general, it was also observed

that the optimal probe annealing temperatures for PCR amplifications was about 5°C higher than the optimal probe hybridization temperature (results not shown). The probes and their optimal annealing temperatures are listed in Table 1. Figure 1 Sections of fluorescent images showing DNA hybridized to the array. Sections of fluorescent images after hybridization of target DNA to the diagnostic array. A. (Top) Hybridization profile of Aspergillus versicolor; (Middle) Penicillium corylophilum; (Bottom) P. expansum. B. The arrangement of a few oligonucleotide probes within the indicated fields of a section of the array. Oligonucleotide probe names were used to indicate BCKDHA the field. Each column represents four replicates of the same spot. Figure 2 Relative intensities of hybridized DNA. Relative intensities after hybridization of labeled target DNA to the array. Each experiment was done in triplicate and the medians and their standard deviations were calculated for each spot on the array. Only positive hybridization results are shown. A. Relative intensities of fungal strains hybridizing to probes designed from the internal transcribed (ITS) regions of Alternaria, Aspergillus, Penicillium and Stenocarpella species. B.

A striking result of this current study was that symbiotic larvae presented a lower immune response to bacterial challenge, when compared to aposymbiotic larvae. Invertebrate immune reactions toward pathogens, and the possible evolutionary impact of endosymbiosis

on shaping these reactions, have been the major focus of research in the past few years [69, 73, 77, 79–81]. The recent genome sequencing of the pea aphid, which shares a long-term symbiotic relationship with the endosymbiont Selleck LY294002 Buchnera, has surprisingly revealed that aphids lack crucial components of the IMD pathway [73]. Furthermore, no apparent AMP was determined by gene annotation [73, 91]. In the same context, Braquart-Varnier et al. [77] have shown that the cellular immune response could be affected by endosymbionts. Isopods harboring Wolbachia (wVulC) exhibited lower haemocyte density and more intense septicaemia in the haemolymph. In the ant, EGFR inhibitor Camponotus fellah, insect treatment with the Rifampin antibiotic resulted in a drastic decrease in the number of symbiotic bacteria, and this

decrease was associated with a higher encapsulation rate when compared with the non-treated insect control [92]. Diminished encapsulation ability in parasitoid Leptopilina eggs has also been reported, in the presence of Wolbachia, in D. simulans [93]. Taken together, these findings lead to the hypotheses that either invertebrate symbiosis may have selected for a simplification of the host immune system or endosymbionts manage to modulate

the host immune expression, presumably for their own survival. A third hypothesis is that invertebrates might allocate different resources to immune pathways. In this case, the relatively low systemic response in weevil symbiotic larvae could be due to the allocation of insect resources to local expression of the bacteriome, to the detriment of the humoral systemic expression. However, although these hypotheses appear to be compatible with our preliminary results on Sitophilus, additional work needs to be done to determine whether decreases in AMP gene expression in symbiotic insects are Janus kinase (JAK) due to endosymbiont manipulation or whether heat-treatment while obtaining apsoymbiotic insects has resulted in a genetic selection of host immunocompetence. Moreover, it is notable that the endosymbiosis interaction with the invertebrate immune system is an emerging field that provides quite contrasting data. Contrary to previous findings, several studies investigating Wolbachia as a potential control agent in vector insect species have reported that Wolbachia can activate the host immune system, and protect the insect against a wide variety of pathogens [79–82]. However, as only a few Wolbachia strains have been tested so far (i.e.

3%] of 420 patients, respectively, experienced a fracture during the study): adjusted OR 1.64 (95% CI 1.16–2.33) for main non-vertebral fractures (also significant for all fractures and all non-vertebral fractures). In a sensitivity analysis of only those patients who completed the 36-month follow-up (n = 991, GSK-3 assay 62.7% of total study cohort), which contained 91% of the total fractures and 73.1% of the total women with an incident clinical fracture during the 36-month follow-up, the results were similar to those for the total study cohort given in Table 2 (data

not shown). Back pain The mean (SD) back pain VAS at baseline was 57.8 (26.6) for the total study cohort. Figure 3 shows the adjusted mean change in back pain VAS from baseline over time. The decrease in pain seen during the 18 months of teriparatide treatment was maintained during the 18 months after teriparatide was discontinued. Of the variables included in the MMRM, three had a significant effect on the change in back pain VAS: each additional 5 mm in baseline VAS was associated with a greater improvement in back pain of −2.89 mm (95% CI −3.07 to −2.71; p < 0.001); a fracture selleck chemicals in the past 12 months before treatment start was associated with a greater improvement in back pain of −2.49 mm (95% CI −4.43 to −0.56; p = 0.012) versus no fracture in the past 12 months; whereas each additional historical fracture

was associated with less improvement in back pain of 1.10 mm (95% CI 0.61 to 1.58; p < 0.001). Fig. 3 Back pain VAS: adjusted mean change (95%

CI) from baseline during and after teriparatide treatment in total study cohort. Data presented is from MMRM analysis. Model included baseline back pain VAS score, number of previous fractures, fracture in 12 months before study entry, age, prior bisphosphonate duration, diagnosis of rheumatoid arthritis, and visit, where repeated measures were modelled with an unstructured correlation matrix. The unadjusted mean (SD) back pain VAS scores at 3, 6, 12, 18, 24, 36 months GNA12 and end of study (LOCF) were 42.9 (25.0), 38.3 (25.4), 34.6 (25.6), 31.9 (25.5), 32.1 (26.7), 29.3 (26.3) and 33.5 (27.3) mm, respectively. The unadjusted mean change from baseline to endpoint was −24.3 (SD 31.9) The results from the back pain questionnaire for the total study cohort are summarised in Table 3. Both the frequency and severity of back pain decreased during teriparatide treatment and this was maintained after teriparatide was discontinued. At every post-baseline visit, there were significantly more patients who reported a decrease compared with an increase in the frequency of back pain relative to baseline (sign test, p < 0.001). The same was true for the severity of back pain (sign test, p < 0.001). The limitations on activities and days in bed due to back pain decreased during the teriparatide treatment and were then maintained in the 18-month post-teriparatide period (Table 3).

P < 0.05 as calculated by the Mann-Whitney's test; *, statistically not significant difference in HCV infectivity compared to infectivity in absence of drugs. Altogether, our data confirm the role of cholesterol in HCV entry and bring to light a similar response of Huh-7w7/mCD81 and Huh-7 cells to cholesterol depletion and replenishment in terms of HCV infection. We next analyzed by flow cytometry the surface expression of CD81 and its association with TEMs in Huh-7w7/mCD81 cells treated with MβCD or MβCD-cholesterol complexes (Figure

6), and expression of CD151 was used as a control (right panels). MβCD treatment of Huh-7w7/mCD81 cells reduced MT81 labelling 3-Methyladenine ic50 by 58 ± 7% (Figure 6Aa), suggesting that cholesterol depletion induced a decrease in total cell surface expression of mCD81 in Huh-7w7/mCD81 cells. Even with cholesterol replenishment, CD81 expression level could not be restored to conditions that would enable HCV infectivity (Figure 6Ac, MβCD+Chol). Incubation of MβCD-treated

cells with increasing concentrations of preformed MβCD-cholesterol complexes raised cell surface mCD81 expression level (Figure 6B). However, a concentration four times higher than needed to reverse the inhibitory effect of MβCD on HCV infectivity (10 mM instead of 2,5 mM) was necessary to reach Selleckchem Talazoparib the cell surface mCD81 expression level of untreated cells. Interestingly, treatment with MβCD alone had no effect on TEM-associated mCD81 population in Huh-7w7/mCD81 cells, as determined using MT81w (Figure 6Ab). Conversely, cholesterol enrichment of non depleted cells with preformed MβCD-cholesterol complexes led to a 2 ± 0.6 fold increase of TEM-associated mCD81 population (Figure 6Af), without any change in the total CD81 population (Figure 6Ae). These results confirm the role of cholesterol in TEM organization. Expression of CD151 under different conditions was not affected (Figure 6A, right panels). Figure

6 Cholesterol depletion affects total CD81 Phosphoprotein phosphatase cell surface expression. A, Flow cytometry analysis of CD81 and CD151 expression on the cell surface of Huh-7w7/mCD81 cells. Upper panels: cells were treated with 7.5 mM of MβCD (MβCD) or left untreated (NT). Middle panels: cells were treated with 7.5 mM of MβCD (MβCD) followed by 2.5 mM of MβCD-Cholesterol (MβCD + Chol). Lower panels: cells were treated with 2.5 mM of MβCD-Cholesterol (Chol) or left untreated (NT). B, Cells were treated with 7.5 mM of MβCD (MβCD) followed by increasing concentrations (in mM) of MβCD-Cholesterol (MβCD + Chol) and total cell surface CD81 expression compared to untreated cells (NT) was measured using MT81 mAb. Our results differ from those of Silvie et al. showing that similar MβCD treatment of Hepa1–6 cells did not lead to a significant decrease of total CD81 cell surface expression [23]. However, it has to be noted that the tetraspanin CD9, expressed in Hepa1–6 cells but not in Huh-7 cells, has been shown to increase stability of tetraspanin complexes [40].

Guo et al. reported that Ni-Zn ferrite thin films exhibit much higher natural resonance frequency, thanks to bianisotropy [13]. There is strong surface anisotropy in ferrite nanoparticles (NPs), which has been reported before [14–16]. Owing to this surface anisotropy, ferrite NPs will likely show high resonance frequency. NiFe2O4 is a typical soft magnetic ferrite with high electrical resistivity

[17], and it is an inverse spinel with metal ions occupying the octahedral and tetrahedral sites. The magnetic moments GSK1120212 in vitro placed in the tetrahedral site and octahedral site couple in an antiparallel manner by a superexchange interaction which is mediated through adjacent oxygen atoms and forms a collinear ferrimagnetic ordering. Additionally, the magnetic behaviors of nanoscale NiFe2O4 are extremely sensitive to their size [18]. There is already

a significant interest in synthesizing NiFe2O4 NPs for achieving optimal magnetic properties [19–21]. In this work, NiFe2O4 NPs were prepared using the sol–gel method. The morphology, structure, and magnetic characterization of the NiFe2O4 NPs have been systemically investigated. Importantly, an adjustable magnetic resonance has been observed in the GHz range, implying that NiFe2O4 is a candidate for microwave devices in the GHz range. Methods NiFe2O4 NPs were synthesized by the sol–gel method with a postannealing process [22]. All chemical reagents used as starting Selinexor supplier materials are of analytical grade and purchased without any further treatment. In a typical synthesis process, 0.01 M Ni(NO3)4·5H2O, 0.02 M Fe(NO3)3·9H2O,

and 0.03 M citric acid were firstly Protein kinase N1 dissolved in 100 ml of deionized water. The molar ratio of metal ions to citric acid was 1. A small amount of ammonia was added to the solution to adjust the pH value at about 7 with continuous stirring. Then, the dissolved solution was stirred for 5 h at 80°C and dried in the oven to form the precursor at 140°C. The precursor was preannealed at 400°C for 2 h and then calcined at different temperatures (700°C, 800°C, 900°C, and 1,000°C) for 2 h in the air, which were denoted as S700, S800, S900, and S1000, respectively. X-ray diffraction (XRD; X’Pert PRO PHILIPS with Cu Kα radiation, Amsterdam, The Netherlands) was employed to study the structure of the samples. The morphologies of the samples were characterized using a scanning electron microscope (SEM; Hitachi S-4800, Tokyo, Japan). The measurements of magnetic properties were made using a vibrating sample magnetometer (VSM; LakeShore 7304, Columbus, OH, USA). The chemical bonding state and the compositions of the samples were determined by X-ray photoelectron spectroscopy (XPS; VG Scientific ESCALAB-210 spectrometer, East Grinstead, UK) with monochromatic Mg Kα X-rays (1,253.6 eV). The complex permeability μ of the particles/wax composites were measured on a vector network analyzer (PNA, E8363B, Agilent Technologies, Inc.