This could be carried out Nutlin-3a in vivo in our future study. The mechanism of NQO1-mediated chemosensitization was further explored. Previous reports suggested that NQO1 modulates p53 expression by interfering with 20S proteasome-mediated

degradation of p53 [24]. Inhibition of NQO1 by dicoumarol suppressed p53 protein levels and induced cell death [24]. In contrast, dicoumarol at non-cytotoxic concentrations, but sufficient to inhibit NQO1 enzyme activity, enhanced p53 protein levels [22]. Present results show that the suppression of NQO1 increased p53 expression. Tumor protein p53 and Bcl family proteins regulate Crenolanib supplier mitochondrial outer membrane permeabilization (MOMP) [26]. Our results showed that the increase of p53 was associated with increased p21 and Bax levels. Both p21 and Bax are p53-dependent downstream gene products. The p21 is a potent cyclin-dependent kinase inhibitor and its expression is associated with the strong antiproliferative effect as was seen in the present study. Bax is a multidomain proapoptotic Bcl2 family. It translocates into the mitochondrial outer membrane and forms Bax pores leading to the release of proapoptotic proteins and ensuing cell death [27]. p53 is a tumor suppressor gene that responded to DNA damage or oxidative

stress by inducing find more growth arrest or apoptotic cell death [28, 29]. Our results showed that knockdown of p53 inhibited the chemosensitizing

effect, which was induced by knockdown of NQO1 in KKU-100 cells. This indicates that the sensitizing effect of NQO1 knockdown is mediated via p53 pathway. It is also noted that KKU-100 cells expressed both the wild type full length p53 as well as the splicing variant of truncated p53 protein [30]. Interestingly, our almost results showed that the potentiation effect of NQO1 gene silencing on the cytotoxicity of chemotherapeutic agents can occur even in cancer cells with high expression ratio of mutant p53/wild type p53. It is yet to determine the chemosensitizing effect of NQO1 suppression on cells expressing the other mutated p53. As some CCA patients express high NQO1 [20], targeting the NQO1 by suppressing the activity or expression could be a strategy to overcome drug resistance of cancer and enhancing the efficacy of chemotherapeutic agents. Conclusions In summary, NQO1 plays an important role in cytoprotection of cancer cells and modulates the sensitivity of chemotherapeutic agents, particularly in the high NQO1 expressing CCA cells. NQO1 is a potential molecular target for enhancing the antitumor activity of chemotherapeutic agents.

The ToxR-like BprP in turn activates genes encoding the structural components of T3SS3, including the araC-type regulatory gene bsaN. BsaN is important for the activation of T3SS3 effector and translocon gene

expression, and several regulatory genes including bprC and virAG, whose gene products control T6SS1 expression [8]. The mechanisms through which these transcriptional regulators control the expression of their target genes are not understood. TGF-beta Smad signaling It is also unclear whether these regulators are acting directly on the identified target genes or through as yet undiscovered intermediary regulators, and whether additional host cell cofactors are involved that may serve as intracellular signals. Compared to T3SSs in other pathogens such as Pseudomonas, Salmonella and Shigella, only a limited number of effectors have been identified for B. pseudomallei T3SS3. One of the effector proteins BI 2536 purchase secreted by T3SS3 is BopE, which is annotated to exhibit guanine nucleotide exchange factor activity and has been reported to facilitate invasion of epithelial cells [15]. bopA is generally assumed to encode a T3SS3 effector since it is located adjacent to bopE, although T3SS3-dependent secretion of BopA has never been verified. Functionally, BopA has been CB-839 mw described to promote

resistance to LC3-associated autophagy and a bopA mutation results in an intracellular DNA ligase replication defect [16,17]. A third effector protein, BopC (BPSS1516), was recently shown to be secreted via T3SS3, and bopC mutants were reported to be less invasive in epithelial cells [18] and to exhibit delayed endosome escape and reduced intracellular growth in J774 murine macrophages [19]. To determine the full extent of the BsaN regulon and examine whether BsaN activates the expression of additional effector genes, we performed global transcriptome analysis of B. pseudomallei KHW wildtype (WT) and a ΔbsaN mutant strain using RNAseq. Our analysis shows that 111 genes are under the direct or indirect transcriptional

control of BsaN. In addition to activating loci associated with T3SS3, we demonstrate that BsaN functions to repress transcription of other loci. Thus, BsaN functions as a central regulatory factor within a more extensive network to facilitate the intracellular lifecycle of B. pseudomallei. Results Identification of the BsaN regulon through RNAseq analysis BsaN (BPSS1546 in the reference B. pseudomallei K96243 genome) was previously shown to function as a central regulator of a hierarchical cascade that activates effector and translocon genes of T3SS3 as well as several associated regulatory genes [8,14]. Furthermore, BsaN was shown to activate the expression of certain T6SS1-associated genes including the two-component regulatory system locus virAG (BPSS1494, 1495), and the bim actin motility genes (BPSS1490-1493).

J Med Microbiol 2012,61(Pt 9):1254–1261.PubMedCrossRef Competing interests The authors have declared that no competing interests exist. Authors’ contributions CF and OP carried out the MCC-950 molecular studies, participated in the MST analysis and drafted the manuscript. HR participated in the molecular studies. CB conceived the design of the study, participated in its design and coordination and drafted the manuscript. All of the authors read and approved the final manuscript.”
“Background Shewanella oneidensis S3I-201 MR-1 is a dissimilatory metal-reducing bacterium [1] and can use

under anoxic conditions insoluble Fe(III) and Mn(IV) oxide minerals as electron acceptors [2, 3]. In the laboratory, S. oneidensis MR-1 forms biofilms under hydrodynamic flow conditions on a borosilicate glass surface, where biofilm formation is mediated by a set of complementary molecular machineries, comprised of the type IV MSHA pilus and a putative exopolysaccharide biosynthesis (EPS) gene cluster (mxdABCD)[4, 5]. The first gene of this cluster is mxdA, www.selleckchem.com/products/kpt-8602.html which is predicted to encode for a gene with unknown function; however, MxdA was recently shown to control

indirectly cellular levels of c-di-GMP in S. oneidensis MR-1 [6]. MxdB has homology to a membrane-bound type II glycosyl transferase and was thought to be involved in the transport of extracellular material involved in forming the matrix of S. oneidensis MR-1 biofilms. This hypothesis was supported by genetic analysis revealing that ∆mxdB mutants were unable to transition from a cell monolayer to a three dimensional biofilm structure [4].

MxdC shares homology with an efflux pump and mxdD was annotated as a conserved hypothetical protein with no known homology. ∆mshA∆mxdB check double mutants were entirely deficient in initial attachment and biofilm formation [5]. Expression of adhesion factors such as EPS are regulated in Vibrio cholerae, Escherichia coli and Pseudomonas aeruginosa in response to environmental factors. The vps gene cluster in V. cholerae, for example, was shown to be controlled in a cell- density dependent manner [7–10] involving several two-component signaling systems (TCS). The global regulator ArcA is part of the ArcS/ArcA two-component regulatory system in S. oneidensis MR-1 [11–14]. Recently, it was shown that phoshorylation of ArcA by ArcS requires the presence of HptA, a separate phosphotransfer domain [14]. HptA of S. oneidensis MR-1 shares homology with the N-terminal domain of ArcB, the sensor histidine kinase of the E. coli ArcB/ArcA system, but does not share significant homology with ArcS from S. oneidensis MR-1. ArcS/HptA have been shown to functionally complement an E. coli ΔArcB mutant [13]. In E.

Otherwise, PC-ADR-Fab exhibit a more CYT387 excellent antitumor ability comparing with PC-ADR-BSA, with 2/4 mice of

complete remission (CR) indicated by no measurable mass. The excellent antitumor activity of our liposome is validated using a disseminated model, in which Daudi cells were transplanted intravenously into SCID mice via tail vein. After 48 h, these mice were randomly administered injections of PBS, free ADR, PC-ADR-BSA, and PC-ADR-Fab for three times once a week. Survival curves were plotted with the Kaplan-Meier method and were compared by using a log-rank test [33, 34]. As illustrated in Figure 6D, ADR-loaded liposome (PC-ADR-BSA and PC-ADR-Fab) treatment significantly prolonged the survival of tumor-bearing mice compared to free ADR and PBS control treatment (*p < 0.05). As our expectation, comparing with PC-ADR-BSA treatment, the administration of PC-ADR-Fab led to significant prolongation of graft survival days (*p < 0.05), with a CR percentage WZB117 datasheet of 4/10 indicated by long-term survival (>120 days post-treatment).

Discussion NHL presents not only as a solid tumor of lymphoid cells in lymph nodes and/or extranodal lymphatic organs, but also as free lymphoma cells in circulating blood [1–3]. Unlike most other malignancies, chemotherapy but not surgery plays the most important role in curing NHL [4–6]. Currently, more and more studies are focusing on finding out novel drug delivery system for treating solid tumors [7, 11, 17, 25]. However, for the elimination of free malignant cells in circulating blood, high serum stability and specificity to tumor cells are of great importance. In this study, we have successfully fabricated a rituximab Fab-conjugated

liposome based on PC, of which the well-defined spherical morphology was observed under TEM. Because PC is a kind of diacetylenic lipids, which can form intermolecular cross-linking through the diacetylenic group by UV irradiation to form chains of covalently linked lipids in the liposomal bilayers (Additional file 1: Figure S1) [26], this covalently union between lipid chains leads to a relatively more compact structure; thus, an important selleck compound impact on the stability of the polymerized drug delivery system can be obtained. This enhanced serum stability can result in longer-time circulation and slower clearance of encapsulated drugs in vivo. Further experimental results revealed a favorable biological compatibility of the liposome. All the abovementioned properties are of vital selleck importance for an ideal drug delivery system in eliminating malignant lymphoma cells, especially those in the peripheral blood. In order to determine the antitumor activities, we took two lymphoma cell lines, Raji and Daudi, as study targets.

9 uidA2 0 0 0 0 O40 3 ET 2 uidA4 0 0 0 0 NT 1 ET 3.1 uidA5 0 0 0 0 NT 3 ET 3.2 uidA5 1 0 0 0 NT 4 ET 3.3 uidA5 1 0 1 0 NT 1 ET 3.4 uidA5 1 0 0 0 O7 click here 13 ET 3.5 uidA5 1 0 1 0 O7 2 ET 3.6 uidA5 0 0 1 0 O7 1 ET 3.7 uidA5 1 0 0 0 O88 1 ET 4 uidA11 0 0 1 0 NT 1 ET 5 uidA20 0 0 0 0 NT 1 ET 6 uidA21 0 0 1 0 NT 1 ET 7 uidA22 0 0 0 0 O15 1 ET 8.1 uidA30 0 0 0 0 O7 1 ET 8.2 uidA30 0 0 1 0 O7 1 ET 8.3 uidA30 1 0 0 0 NT 1 ET 9.1 uidA50 0 0 1 0 NT 2 ET 9.2 uidA50 0 0 0 0 O15 1 ET 10.1 uidA55 0 0 0 0 NT 2 ET 10.2 uidA55 0 0 1 0 NT 1 ET 11 uidA57 0 0 0 0 O8 1 ET 12 uidA65 0 0 1 0 NT 4 ET 13 uidA66 0 0 1 0 O26 1 ET

14.1 uidA90 0 0 0 0 O150 8 ET 14.2 uidA90 0 0 0 0 O15 3 ET 14.3 uidA90 0 0 0 1 O26 1 ET 15 uidA103 0 0 0 0 NT 1 ET 16 uidA110 0 0 0 0 NT 3 ET 17.1 uidA111 0 0 0 0 NT 3 ET 17.2 uidA111 0 0 1 1 NT 1 ET 17.3 uidA111 0 1 1 1 NT 1 ET 18 New allele 1 0 0 1 O7 1 aAMX: amoxicillin; CHL: chloramphenicol; TET: tetracyclin; all of epidemiological buy GSK2118436 types of E. The binary coding stands for presence (1) or selleck chemical absence (0) of hly gene amplification, and resistance (1) or non-resistance (0) to antibiotics. Figure 3 Distribution of E. coli B1 epidemiological types in relation to hydrological conditions (A) and before and after a rain event during a wet period (B). In the most contaminated water (4.0 ± 0.7 104 CFU/100 ml), the diversity of E. coli B1 strains (i.e., number of ETs/total number of B1 isolates for the sampling campaign) was higher (12/15) than in less contaminated water (9/17 in water containing 1.0 ± 0.1 102 CFU/100 ml; 12/39 in water containing 6.2 ± 0.6 102 CFU/100 ml) (Figure 3A). At the peak of the turbidity, E. coli density reached a value of 7.2 102 CFU/100 ml, the diversity of E. coli B1 strains was higher (6/6) than the diversity observed when turbidity and E. coli density decreased (10/29) (Figure 3B). Among the 40 ETs, strains

of the group ET1.1 were present in all samples, regardless of the hydrological condition or the current land use in the watershed. However, they made up a greater proportion of the strains under non-storm conditions: during the dry period (no contribution Paclitaxel of fecal bacteria from the watershed), 13 ET1.1/39 E.

The entire system of the human gut microbiota functions as a ‘microbial organ’ within

the intestine, which contributes to diverse mammalian processes including protective functions against E7080 chemical structure pathogens and immune-system modulation, the metabolic function of fermenting non-digestible dietary fiber, anaerobic metabolism of peptides and proteins that results in the recovery of metabolic energy for the host [7]. The microbial diversity of the human gut is the result of co-evolution between microbial communities CP673451 and their hosts. Microbial community structure is a very important factor that can influence predisposition to specific diseases in certain host contexts [8]. Ingestion see more of the cyst of E. histolytica through fecally contaminated food or water initiates infection. Excystation in the intestinal lumen produces trophozoites and colitis results when the trophozoites penetrate the mucus layer and damages intestinal tissues [9]. The trophozoites proliferate in lumen and phagocytose

resident flora. E. histolytica trophozoites are quite selective in respect to their interactions with different bacterial species and only those bacteria which have the appropriate recognition molecules get attached and ingested [10]. It has been observed that the nuclear DNA content of E. histolytica trophozoites growing in axenic cultures is at least 10 fold higher than in xenic cultures and re-association of axenic cultures with their bacterial flora led to a reduction of DNA content attaining the original xenic values indicating a flexible nature of the parasite genome [11]. Fluctuations in gut flora have been reported both in acute diarrhea and antibiotic associated diarrhea [12], but very few reports are available on status of gut flora

in E. histolytica infected individuals. Earlier studies in our laboratory [1] have recorded fluctuations in the gut flora by a qualitative method during LY294002 disease conditions. 5-Nitroimidazole drugs are still used as first line of defense against amoebic and other infections caused by anaerobes. These drugs are administered as pro drugs and one electron reduction of nitro group converts the pro drug into an active drug [13]. Enzymatic modification mediated by nim-class of genes is a well characterized resistance mechanism. Certain Bacteroides species which are members of the normal colonic human microflora harbor nim genes [14]. Our study is based on the hypothesis that the Entamoeba histolytica (but not E. dispar) is an invasive organism and invades the mucus layer and subsequently the intestinal epithelium for colonization using the pathogenic factors.

albicans transition from yeast form to hyphal phenotype. Yeast cultures supplemented with 10% FBS and the KSL-W peptide were maintained for

various incubation periods. As shown in Figure 2, germ tube formation was inhibited as early as 4 h following exposure to the peptide, compared to that in the cultures incubated in the absence of KSL-W. Of interest is the elevated number of C. albicans hyphal forms in the negative control culture (no KSL-W or amphotericin B) compared to the low number in the ACY-738 presence of KSL-W. The effect of this antimicrobial peptide on C. albicans transition was also dose-dependent: at 1 μg/ml, a significant see more number of hyphal forms remained, and at only 5 μg/ml of KSL-W, C. albicans transition was completely inhibited (Figure 2). Semi-quantitative analyses using inverted microscope observations to estimate the hyphal forms confirmed the inhibited C. albicans transition when treated with KSL-W (Table 1). The density of the hyphae was reduced as early as 4 h of contact with 5 μg/ml of KSL-W. This effect was further supported when C. albicans was placed in contact with KSL-W for 8 h (Table 1), thus confirming that KSL-W downregulated C. albicans growth and transition. Figure 2 KSL-W inhibited C. albicans

yeast-to-hyphae transition. C. albicans was cultured in Sabouraud medium buy 4SC-202 containing 10% fetal bovine serum with or without KSL-W at various concentrations and was maintained for 4 and 8 h at 37°C. After each time point, the cultures were observed under an inverted microscope and photographed. Representative photos of the morphological changes after 4 h of culture are presented. Table 1 Estimation of hyphae forms in the C. albicans culture Active molecules Concentration (μg/mL) Transition at 4 h Transition at 8 h Negative control 0 ++ ++ KSL-W 1 ++ ++   5 – -   10 – -   15 – -   25 – -   100 – - Amphotericin B 1 – - This Table depicts the presence of hyphae following 4 and 8 h treatments of C. albicans

with and without KSL-W or amphotericin B. (–) refers to the absence hyphae form, and (++) refers to the presence high number of hyphae forms. These data were estimated after evaluation over 20 fields from each culture condition, by two independent BCKDHA and blinded examiners. KSL-W reduced C. albicans biofilm formation As KSL-W contributed to reducing C. albicans growth and transition, we sought to determine whether it also displayed inhibitory activity against C. albicans biofilm formation. Using a biofilm-promoting scaffold, SEM analyses, and an XTT assay, we were able to demonstrate the inhibitory effect of KSL-W on biofilm formation (Figure 3). SEM analyses revealed a significant density of C. albicans in the untreated culture, compared to a lower density in the scaffold in the presence of KSL-W (1 and 25 μg/ml) after 4 days of culture.

From January to July 2005, patients undergoing surgery/interventional drainage for IAIs with a positive microbiological culture were included by 25 French centers. A total of 829 microorganisms were cultured. In this study the number of peritoneal microorganisms per sample was ≥3

in 34% and 54% of cases, respectively, for community-acquired and nosocomial infections (P < 0.001). The distribution of the microorganisms differed according to the nosocomial or community origin of the infection but not according to their location (data not shown). In nosocomial patients, increased proportions of Enterococcus faecalis (33% versus 19% in community-acquired patients; P < 0.05) and Pseudomonas learn more aeruginosa Idasanutlin ic50 strains (13% versus 5% in community-acquired patients; P < 0.01) were observed. Conversely, in nosocomial patients, decreased proportions

of Escherichia coli (52% versus 72% in community-acquired patients, P < 0.001) and streptococci strains were reported (31% versus 50% in community-acquired patients, P < 0.01). Therefore the inclusion of anti-enterococcal drugs in any empirical antibiotic regimens in severe nosocomial IAIs and/or in patients with well known risk factors, seems appropriate, mainly if directed against E. faecalis. Empiric therapy directed against vancomycin-BAY 63-2521 solubility dmso resistant Enterococcus faecium is not recommended unless the patient is at very high risk for an infection due to this organism, such as a liver transplant recipient with an intra-abdominal infection Dichloromethane dehalogenase originating in the hepatobiliary

tree or a patient known to be colonized with vancomycin-resistant E. faecium. Enterococcus infections are difficult to treat because of both intrinsic and acquired resistance to many antibiotics. Enterococci are intrinsically resistant to many penicillins, and all cephalosporins with the possible exception of ceftobiprole and ceftaroline, currently undergoing clinical evaluation. Besides Enterococci have acquired resistance to many other classes of antibiotics, to which the organisms are not intrinsically resistant, including fluoroquinolones, aminoglycosides, and penicillins. Many strains of E. faecalis are susceptible to certain penicillins and glycopeptides; however, some strains of E. faecium may be resistant to these agents [272]. Vancomycin-resistant Enterococcus (VRE) infections have been associated with increased morbidity and mortality [273, 274]. Many factors can increase the risk of colonization with VRE. These include previous antibiotic therapy (the number and duration of antibiotics received) prolonged hospitalization, hospitalization in an intensive care unit severity of illness, invasive procedures and devices, gastrointestinal surgery, transplantation, proximity to another VRE-positive patient [275].

The fact that viruses are more abundant than their targets is not surprising, since every single cellular species is infected by many diverse viral species

(as we know very well from the case of our own species, Homo sapiens) and the infection of a single cell always produces a high number of viral particles. However, the data have impressed biologists and contributed find more to a renewal of interest in virus research. The ecology of viruses, their roles in major geochemical cycles, and in controlling the diversity of population are now active research fields (Suttle 2007). Surprising Diversity in the Morphology of Viral Particles Our initial view was that of a curious but monotonous world. Viruses (confused with viral particles, see below) were essentially either small spheres (sometimes with spikes as in TV cartoons featuring the AIDS virus), or

strange Lunar exploratory module (LEM) with a head, a tail, and sometimes legs (as in the case of the T4 bacteriophage and related myoviridae). Specialists (virologists) were aware of the existence of filamentous viral particles, or pleomorphic types of capsids (as in the case of vaccinia or poxviruses), but these were CBL-0137 manufacturer considered as exceptions. This has changed now, with the discovery, during the last two decades, that viruses infecting hyperthermophilic archaea (members of the third domain of life, see below) produce viral particles with a morphology that is completely different from the GSK690693 in vivo classical head and tailed structure of bacteriophages (Prangishvili et al. 2006). Some of their virions are either flexible or rigid filaments that superficially D-malate dehydrogenase resemble those of viruses infecting bacteria or eukarya, but they form clearly distinct families (for instance, they are all double-stranded DNA viruses, whereas eukaryotic filamentous viruses are all RNA viruses). Other viral particles show morphotypes previously never seen in the viral world, such as lemon-shaped, or bottle-like structures. The most spectacular example is the virus ATV (Acidianus-Tailed-Virus) whose virion undergoes the first known case of extra-cellular development (Häring et al. 2005). The virions produced by

ATV infected cells are lemon-shaped particles that can be stored for months at room temperature without any change in their morphology. However, as soon as there are incubated at high temperature (above 70°C) they undergo a drastic structural reorganization, with the formation of two long tails at opposite ends of the central body (Häring et al. 2005). A New Virus Classification Inferred from the Three Domains Concept The unique archaeal viruses, isolated from terrestrial hot springs and infecting organisms living at temperatures between 79 and 105°C, are not just mere curiosities. Their discovery has led to revise the classification of viruses and their relation to cellular organisms. Traditionally, viruses have been classified according to the prokaryote/eukaryote dichotomy.

PA and PM are PhD students in the group. Acknowledgements Regarding simulations with the finite element method, the collaboration with Frank Schmidt’s group from the Zuse-Institut Berlin is acknowledged. Funding from the Helmholtz-Association for Young Investigator groups within the Initiative this website and Networking fund (VH-NG-928) is greatly acknowledged. Electronic supplementary material Additional file 1: Figure S1: Absorption cross section of a 120-nm radius Ag nanoparticle

with dielectric function according to a Drude fit: sum and allocation to different modes. (JPEG 1 MB) Additional file 2: Figure S2: Map of scattering cross section for a spherical dielectric www.selleckchem.com/products/3-methyladenine.html nanoparticle with n = 2 and k = 0. (PNG 131 KB) Additional file 3: Figure S3: Maps of (a) scattering cross section and (b) scattering efficiency for a spherical nanoparticle from GZO semiconductor (refractive index data fitted with parameters from [27]). (TIFF

287 KB) Additional file 4: Figure S4: Scattering cross section of a Ag nanoparticle (fitted with Drude model) of r =120 nm in vacuum and when placed onto a substrate with n = 1.5. (JPEG 835 KB) References 1. Mie G: Beitrage zur Optik truber Medien, speziell kolloidaler Metallosungen. Annalen der Physik 1908,3(25):377–445.www.selleckchem.com/products/vx-661.html CrossRef 2. Walters G, Parkin IP: The incorporation of noble metal nanoparticles into host matrix thin films: synthesis, characterisation and applications. Journal of Materials Chemistry 2009,19(5):574–590.CrossRef 3. Gu X, Qui T, Zhang W, Chu PK: Light-emitting diodes enhanced by localized surface plasmon resonance. Nanoscale Research Letters 2011, 6:199/1–199/12.CrossRef 4. Maier SA, Kik PG, Atwater HA,

Meltzer S, Harel E, Koel BE, Requicha AA: Local detection of electromagnetic energy transport below the diffraction limit in metal nanoparticle plasmon waveguides. Nature selleckchem Materials 2003,2(4):229–232.CrossRef 5. Dregely D, Taubert R, Dorfmüller J, Vogelgesang R, Kern K, Giessen H: 3D optical Yagi-Uda nanoantenna array. Nature Communications 2011, 2:267/1–267/7.CrossRef 6. Nie S, Emory SR: Probing single molecules and single nanoparticles by surface-enhanced Raman scattering. Science 1997,275(5303):1102–1106.CrossRef 7. Lee KG, Kihm HW, Kihm JE, Choi WJ, Kim H, Ropers C, Park DJ, Yoon YC, Choi SB, Woo DH, Kim J, Lee B, Park QH, Lienau C, Kim DS: Vector field microscopic imaging of light. Nature Photonics 2007,1(1):53–56.CrossRef 8.