Sensitivity of the decision tree was defined as the number of patients with PLTEs in the high- and intermediate-risk groups over the total number of patients with PLTEs. Finally, we assessed the performance

of the decision tree in the validation dataset. Results Characteristics of the study patients At the five study centers, 574 of about 992 eligible patients completed the SAQ-GE. Among them, 516 met our inclusion criteria and were entered into the study. A final diagnosis of PLTE was made in 145 (28.1%) patients. Table 1 lists the main patient characteristics and diagnoses in the overall population of 516 patients, of whom 344 were randomly allocated to the derivation dataset and 172 to the validation dataset. PLTEs were diagnosed in 96 (27.9%) derivation-dataset patients and 49 (28.5%) validation-dataset patients. Patient characteristics were not significantly different in the two datasets (data not shown). Table 1 Characteristics SIS3 Navitoclax order and main diagnoses in the study patients   Overall population N = 516 PLTE N = 145 Other N = 371 Age in years, mean ± SD 31.6 ± 7.7 30.7 ± 7.9 31.9 ± 7.6 Gravidity, median [range] 2 [0–11] 2 [0–9] 2 [0–11] Parity,

median [range] 1 [0–7] 1 [0–4] 1 [0–7] Contraception, n/N (%) 136/504 (27.0) 40/141 (28.4) 96/363 (26.5) NRS pain score at admission, mean ± SD 6.4 ± 2.7 6.8 ± 2.7 6.2 ± 2.7* Diagnosis       Ectopic pregnancy, n (%) 148 (28.7) 77 (53.1) 71 (19.1) Pelvic inflammatory disease, n (%) 73 (14.1) 25 (17.2) 48 (12.9) Uncomplicated ovarian cyst, n (%) 70 AMP deaminase (13.6) NA 70 (18.9) Adnexal torsion, n (%) 31 (6.0) 31 (21.4) NA Appendicitis, n (%) 6 (1.2) 6 (4.1) NA Ruptured cyst with hemoperitoneum > 300 mL, n (%) 5 (1.0) 5 (3.5) NA Miscarriage, n (%) 79 (15.3) NA 79 (21.3) Myoma necrobiosis, n (%) 15 (2.9) NA 15 (4.0) Urologic disease, n (%) 10 (1.9) NA 10 (2.7) Ovarian hyperstimulation, n (%) 7 (1.4) NA 7 (1.9) Other diagnosis, n (%) 72 (13.9) 1 (0.7)‡ 71 (19.1) PLTE, potentially life-threatening emergencies; NRS, selleck screening library numerical rating scale for pain

severity; NA, not applicable; SD, standard deviation. *P < 0.05, Student’s t test; ‡Intestinal obstruction. Main results Table 2 reports the results of the univariate analysis. None of the SAQ-GE items had Lr + values greater than 4 or Lr- values lower than 0.25.Figure 1 shows the decision tree, in which three items are taken into account sequentially: vomiting, sudden onset of pain, and pain upon self-palpation. Patients with no vomiting or pain upon palpation are at low risk, with a probability of PLTE of 13% (95% CI, 6%-19%). The intermediate risk group is defined based on either no vomiting but pain upon self-palpation or vomiting but no sudden onset of pain; the probability of a PLTE is 27% (95% CI, 20%-33%). In the high-risk group, with both vomiting and sudden-onset pain, the probability of a PLTE is 62% (95% CI, 48%-76%), ruling out PLTE with a specificity of 92.

Second, the highly inhomogeneous arrangement of GNRs in thin GNR-OPC films can produce more electromagnetic hot spots. Finally, additional contribution can come from multiple scattering within thick opal films, though this assumption needs to be specially studied. Conclusions In this work, we have studied a very simple technique to fabricate SERS substrates using wet chemical approaches only.

Our approach is based on the use of a plasmonic powder of gold nanorods that are CUDC-907 in vitro applied in a concentrated form onto an opal-like substrate of silicon nanospheres. As compared with the previously studied randomly oriented mono- and polylayers of gold nanorods on a plain silicon substrate, the structures obtained by us provide for a two- to fivefold enhancement of the SERS signal. The main mechanisms behind this effect are apparently the increase of the number of reporter molecules adsorbed on the mesoporous substrate and the increase of the number of electromagnetic hot spots. Of course, the selleck chemical analytical SERS enhancement coefficients selleck chemicals llc attained with our

structures are a few orders of magnitude lower than those for such structures as the silver-immobilized nanorod assembly [41, 42]. However, the principal advantage of our approach is its exceptional simplicity, for it requires no special procedures of vacuum deposition on colloidal crystals. Several ways are possible to optimize the method described here. First, it seems advisable to replace gold nanorods with silver-coated nanorods [63] or to investigate other types of nonspherical gold or silver nanoparticles [64]. For example, Zhang et al. [65] fabricated SERS substrates

based on large-scale metallic thin films assembled from size-selected silver nanoplates with tunable plasmonic properties. It was shown [65] that the aggregation of silver nanoplates with sharp corners produces hot spots between the corner gaps, thus Y27632 leading to strong electromagnetic SERS enhancement. Unfortunately, unlike that of gold nanorods, the high-yield fabrication of monodisperse silver nanorods is not an easy task [66, 67], and a recent review of this issue has been published by Negri and Dluhy [68]. However, gold nanorods can be used as convenient templates for subsequent silver coating to ensure flexible tuning of the localized plasmon resonance from near-infrared (e.g., 900 nm) to visible (e.g., 580 nm) [69]. Our preliminary results show that the Au@Ag core-shell nanorod assemblies demonstrate better SERS performance as compared to aggregated gold nanorod films. Our full 3-D finite-difference time-domain simulations [70] confirm the existence of enhanced local electromagnetic hot spots that are more intensive in the case of random assemblies of silver-coated nanorods. Investigations along these lines are under way at our laboratories, and the results will be published elsewhere.

Watanabe H, Shimotani K, Shigematu T, Manabe C: Electric measurements of nano-scaled devices. Thin

Solid Films 2003, 438:462–466.CrossRef 72. Amman M, Ben-Jacob E, Mullen K: Charge solitons in 1-D array of mesoscopic tunnel junctions. Phys Lett A 1989,142(6):431–437.CrossRef 73. Gupta RK, Saraf V: Nanoelectronics: tunneling current in DNA–single electron transistor. Curr Appl Phys 2009,9(1):S149-S152.CrossRef 74. Wikipedia: Akane, Phosphodiester Bond of DNA. San Francisco; 2008. 75. Yan H, Zhang X, Shen Z, Seeman NC: A robust DNA mechanical device controlled by hybridization topology. Nature 2002,415(6867):62–65.CrossRef Selleckchem GANT61 76. Joyce DM, Venkat N, Ouchen F, Singh KM, Smith SR: Grote JG. MRS Proceedings: DNA-Based hybrids for energy

storage applications; 2012. 77. Nakamura K, Ishikawa T, Nishioka D, Ushikubo T, Kobayashi N: Color-tunable multilayer organic light emitting diode composed of DNA complex and tris (8-hydroxyquinolinato) aluminum. Appl Phys Lett 2010,97(19):193301–1-193301–3.CrossRef 78. Wang G, Tanaka A, Matsuo Y, Niikura K, Ijiro K: DNA-templated self-assembly of conductive selleck chemical nanowires. In Design for Innovative Value Towards a Sustainable Society. Edited by: Matsumoto M, Umeda Y, Masui K, Fukushige S. New York: Springer; 2012:911–914.CrossRef 79. ABT-888 manufacturer Li Y, Kaneko T, Hatakeyama R: Formation of quantum dots in single stranded DNA-wrapped single-walled carbon nanotubes. Appl Phys Lett 2010,96(2):023104–1-023104–3. 80. Park SJ, Taton TA, Mirkin CA: Array-based electrical detection of DNA with nanoparticle probes. Science 2002,295(5559):1503–1506. 81.

Cai H, Cao X, Jiang Y, He P, Fang Y: Carbon nanotube-enhanced electrochemical DNA biosensor for DNA hybridization detection. Anal Bioanal Chem 2003,375(2):287–293. 82. Patolsky F, Timko BP, Yu G, Fang Y, Greytak AB, Zheng G, Lieber CM: Detection, stimulation, and inhibition of neuronal signals with high-density nanowire transistor arrays. Science 2006,313(5790):1100–1104.CrossRef 83. Cai H, Xu C, He P, Fang Y: Colloid Au-enhanced DNA SDHB immobilization for the electrochemical detection of sequence-specific DNA. J Electroanal Chem 2001,510(1):78–85.CrossRef 84. Le JD, Pinto Y, Seeman NC, Musier-Forsyth K, Taton TA, Kiehl RA: DNA-templated self-assembly of metallic nanocomponent arrays on a surface. Nano Lett 2004,4(12):2343–2347.CrossRef 85. Kulkarni A, Amin R, Kim H, Hong BH, Park SH, Kim T: Photoresistivity and optical switching of graphene with DNA lattices. Curr Appl Phys 2011,12(3):623–627.CrossRef 86. Kim J, Kasture M, Hwang T, Kulkarni A, Amin R, Park S, Kim T, Gosavi S: Graphene-based waveguides: novel method for detecting biological activity. Appl Biochem Biotechnol 2012,167(5):1069–1075.CrossRef 87. Carr PA, Park JS, Lee YJ, Yu T, Zhang S, Jacobson JM: Protein-mediated error correction for de novo DNA synthesis. Nucleic Acids Res 2004,32(20):e162-e162.CrossRef 88.

Therefore, the ability of vaccines to elicit effective antitumor immunity was impaired. CY has immunomodulatory effects, and low-dose CY (20 mg/kg) was found to selectively deplete CD4+CD25+ T cells (Treg) and impede the tolerance [42]. CY can preconditioning enhance the CD8+ Selleck GDC-0449 T-cell response to peptide vaccination, thus

leading to enhanced antitumor effects against pre-existing tumors [43]. Cy markedly enhanced the magnitude of secondary but not primary CTL response induced by vaccines and synergized with vaccine in therapy but not in prophylaxis tumor models [44]. With our enhanced vaccine, IFN-γ secretion was significantly increased. In addition, CD8+ and NK cells were triggered

to release IFN-γ and mediate cytotoxic activity. The increased IFN-γ secretion may also be due to the combined effects of HSP60 in mHSP/P and IL-12. Hsp60-inducing IFN-γ depends strictly on the ability of the macrophages to click here produce IL-12 [45]. Activation and expansion of tumor-specific T cells by HSP/Ps were identified [46]. Our study showed that mHSP/Ps purified C59 wnt manufacturer from S180 sarcoma cells activated tumor antigen-specific T cells in vitro, and the induction of tumor-specific CTLs with enhanced vaccine was stronger than that with mHSP/Ps alone, possibly because of the combined effect of HSP60 and IL-12. HSP60 induces a strong non-specific immune reaction, but when it meets IL-12, it can activate cytotoxic T cells. HSP60 can mediate the activation of cytotoxic T cells, which depends on production of IL-12

[47]. Our data showed that inflammatory cells infiltrated tumors with mHSP/P vaccination and that a preexisting antitumor immune response was elicited, which was required for an effective IL-12 response for tumor rejection. Conclusions To enhance the current immunotherapeutic efficacy, novel strategies designed in the laboratory and proven in preclinical Casein kinase 1 animal tumor models are now entering the clinic trials [48, 49]. These novel strategies involved breaking tolerance to tumor self-antigens by inhibiting regulatory T cells, boosting T-cell co-stimulation and using combinations of recombinant cytokines and other defined molecules with “”immuno-enhancing”" activities. Our immunization protocol of a combination immunotherapeutic regimen of vaccination with mHSP/Ps followed by low-dose CY plus IL-12 resulted in enhanced immunologic antitumor activity that was better than that of either treatment alone. Acknowledgements and Funding This study was supported by the National High Technique Research and Development Program of China funded by the Chinese government (863 No. 2007AA021806). We are thankful of Dr.

b Inference of gene regulatory networks using hip BMD genes

Discussion GWA is a powerful tool that can identify genes associated with common diseases or traits such as BMD variation. Nonetheless, GWA studies usually focus on the most significant individual variants without considering the global evidence of the gene tested. It should be noted that allelic heterogeneity (i.e., presence of more than one susceptibility allele in a locus or gene) greatly reduces the power for testing of an individual SNP [7, 8]. Therefore, a gene-based test can ameliorate the situation by simply testing the global null hypothesis about the SNPs located per gene. The gene-based test is a direct and powerful means of protecting the overall false-positive rate when a collection of loci are tested, because the p value from the gene-based test has already corrected the number of SNPs included via a simulation approach. Using gene-based analysis selleck products of GWA data, our study confirmed several well established candidate genes and suggested several novel genes and loci for BMD variation. MM-102 chemical structure Importantly, most of these genes did not contain any SNP that reached genome-wide significance, so the potential importance of these genes would not have been recognized in the absence of gene-based association study. An ethnic-specific BMD gene may underlie BMD variation in southern Chinese and

Europeans. In line with the observations of our recent GWAS, there was no Selleck ARS-1620 overlap of genes in the significant or suggestive gene list from HKSC and dCG populations We recently identified a SNP rs2273601 in JAG1 that was associated with spine BMD (p value = 1.06 × 10−8) in 1,520 HKSC subjects with extreme BMD; nonetheless, only a modest association of this SNP with spine BMD was observed in three Caucasian cohorts (p range, 0.007–0.045) [3]. In the current study, we observed that top hip BMD genes were more consistent in HKSC and dCG, as reflected by the inflation factor and the results from independent t testing (Supplementary methods, Supplementary Figures 3 to 4, and Supplementary Table 2). The discrepancies of gene-based association results for spine ALOX15 BMD in two populations

may be due to a number of factors such as lifestyle, diet, and genetic background. Although these factors may also affect hip BMD, the possibility that spine BMD may be more susceptible than hip BMD to gene and environment interaction cannot be excluded. If this hypothesis is true, identification of gene and environmental interaction will benefit genetic research into osteoporosis and clinical practice. The study design of HKSC and dCG also differed. In our HKSC cohort, we studied subjects at the extremes of BMD distribution. Studying subjects at the extremes of a quantitative phenotype has proven useful in identifying functional rare variants [9, 10]. The genes identified in our HKSC cohort may therefore harbor more rare variants than the dCG cohort.

Nucleic Acids Res 1999,27(1):49–54.PubMedCentralPubMedCrossRef 31. Boeckmann B, Bairoch A, Apweiler R,

Blatter MC, Estreicher A, Gasteiger E, Martin MJ, Michoud K, O’Donovan C, Phan I, et al.: The SWISS-PROT protein knowledgebase and its supplement TrEMBL in 2003. Nucleic Acids Res 2003,31(1):365–370.PubMedCentralPubMedCrossRef 32. Cantarel BL, Coutinho PM, Rancurel C, Bernard T, Lombard V, Henrissat B: The Carbohydrate-Active EnZymes selleck compound database (CAZy): an expert resource for Glycogenomics. Nucleic Acids Res 2009,37(Database issue):D233-D238.PubMedCentralPubMedCrossRef 33. Winnenburg R, Baldwin TK, Urban M, Rawlings C, Kohler J, Hammond-Kosack KE: PHI-base: a new database for pathogen host interactions. Nucleic Acids Res 2006,34(Database issue):D459-D464.PubMedCentralPubMedCrossRef SB-715992 datasheet 34. Chakraborty A, Ghosh S, Chowdhary G, Maulik U, Chakrabarti S: DBETH: a database of bacterial exotoxins for human. Nucleic Acids

Res 2012,40(Database issue):D615-D620.PubMedCentralPubMedCrossRef 35. Chen L, Yang J, Yu J, Yao Z, Sun L, Shen Y, Jin Q: VFDB: a reference database for bacterial virulence factors. Nucleic Acids Res 2005,33(Database issue):D325-D328.PubMedCentralPubMedCrossRef 36. Delcher AL, Salzberg SL, Phillippy AM: Using MUMmer to https://www.selleckchem.com/products/Romidepsin-FK228.html Identify Similar Regions in Large Sequence Sets. 2003. [Current Protocols in Bioinformatics/Editoral Board, Andreas D Baxevanis [et al.] 2003, Chapter 10:Unit 10 13] 37. Lemeer S, Hahne H, Pachl F, Kuster B: Software tools for MS-based quantitative proteomics: a brief overview. Methods Mol

Biol 2012, 893:489–499.PubMedCrossRef 38. Greenbaum D, Jansen R, Gerstein M: Analysis of mRNA expression and protein abundance data: an approach for the comparison of the enrichment of features in the cellular population of proteins and transcripts. Bioinformatics 2002,18(4):585–596.PubMedCrossRef 39. Zhang W, Culley DE, PAK5 Scholten JC, Hogan M, Vitiritti L, Brockman FJ: Global transcriptomic analysis of Desulfovibrio vulgaris on different electron donors. Antonie Van Leeuwenhoek 2006,89(2):221–237.PubMedCrossRef 40. Nie L, Wu G, Culley DE, Scholten JC, Zhang W: Integrative analysis of transcriptomic and proteomic data: challenges, solutions and applications. Crit Rev Biotechnol 2007,27(2):63–75.PubMedCrossRef 41. Crick F: Central dogma of molecular biology. Nature 1970,227(5258):561–563.PubMedCrossRef 42. Gygi SP, Rochon Y, Franza BR, Aebersold R: Correlation between protein and mRNA abundance in yeast. Mol Cell Biol 1999,19(3):1720–1730.PubMedCentralPubMed 43. Lleo MM, Fontana R, Solioz M: Identification of a gene (arpU) controlling muramidase-2 export in Enterococcus hirae. J Bacteriol 1995,177(20):5912–5917.PubMedCentralPubMed 44. Stieglmeier M, Wirth R, Kminek G, Moissl-Eichinger C: Cultivation of anaerobic and facultatively anaerobic bacteria from spacecraft-associated clean rooms. Appl Environ Microbiol 2009,75(11):3484–3491.

2). Moreover, sensitization to TX in KF-TX cells by CLU-siRNA was further confirmed after time dependent fashion of TX treatment by FACS analysis (at 36, 48 and 60 h; Figure 5C.1) where dead cells indicated by the sub diploid G0 cells. Further confirmation for differential apoptotic cells

was obtained by Annexin V staining (Figure 5C.2). These data indicate that response to TX administration is enhanced after CLU-siRNA transfection. In addition, a dose dependent enhancement of apoptosis by TX in KF-TX cells after CLU knock-down was verified by DNA laddering experiment (data not shown). On the other hand, cellular viability was studied under experimental conditions similar to this https://www.selleckchem.com/products/lgk-974.html described above PXD101 supplier except that OGX-011 was used to knock down CLU while control oligodeoxynucleotide was used for control transfection. Figure 6A shows significantly less viability of KF-TX cells pre-treated with OGX-011 and TX than those pre-treated with control oligodeoxynucleotide and TX. Similarly, sensitization to TX in KF-TX cells by OGX-011 was further confirmed by FACS analysis (Figure 6B). Further confirmation for Torin 2 concentration differential apoptotic cells was obtained by Annexin V staining (Figure 6C). Together, the aforementioned data indicate that silencing s-CLU by specific siRNA or

OGX-011 enhanced TX toxicity in the ovarian cancer cells. Figure 6 Targeting CLU by OGX-011 sensitizes ovarian cancer cells to TX treatment. A.Comparative viability of chemoresistant ovarian cancer cells before and after CLU knock down by OGX-011. Cells were cultured in 96-well plates, then transfected Methane monooxygenase either with CLU-siRNA or control siRNA twice. Twenty-four hours after last transfection, cells were treated with TX. Seventy-two hours after drug addition at indicated doses, cell viability was estimated. KF-TX cells showed enhanced

TX-induced toxicity in CLU KD cells versus controls. B. A representative time-dependent DNA histogram (FACS analysis) demonstrating that CLU KD by OGX-011 at 1200 nM enhanced TX toxicity in KF-TX cells. KF-TX cells were transfected either with OGX-011 or control Oligonucleotide and then challenged with TX dose of 200 nM at indicated time periods (24 h, 36 h,48 h and 60 h). B. Results of Annexin V staining of cells pre-treated with OGX-011 at different concecntrations (400, 800 and 1200 nM) then treated with TX (200 nM) for indicated time periods (24, 48 and 72 h). Quantification of the relative ratio of apoptotic cells at different time points indicated the significant enhancement of TX toxicity by OGX-011. The maximum enhancement was obtained by 800 nM OGX-011 while the conc. of 1200 nM did not show further significant improvement in toxicity. D. CLU knock down modulates cellular growth rate of ovarian cancer cells. (1) KF-TX cells showed enhanced growth rate when transfected with CLU siRNA with regard to controls.

Comparable levels of hBD2 were detected in the supernatants of all cells exposed to SC: 100, 180 and 70 pg/ml were found in the supernatants of 16HBE, HNT and A549 cells, respectively, which was statistically significantly higher then hBD2 levels in the supernatants of the cells alone or the cells exposed to RC, HF or latex beads. Exposure of any cells to RC or HF resulted in lower levels of hBD2, ranging from 20 to 70 pg/ml. The difference between hBD2 levels in the supernatants of the see more cells exposed to either RC, or those exposed to latex beads, was statistically significant for HNT cells, while this difference did not reach statistically

a significant level for A549 and 16HBE cells. This could be explained by the different Belnacasan reactions of the different kinds of cells to the pathogen. The difference between hBD2 levels in the supernatants of 16HBE, HNT and A549 cells exposed to either RC, or those exposed to latex beads, was statistically insignificant. Figure 9 Analysis of hBD2 level in cell supernatants. The level of hBD2 in supernatants of 16HBE, A549 and primary culture HNT cells was measured by sandwich-ELISA. Briefly, cells were grown and exposed to different A. fumigatus organisms, latex beads or Il-1β (Ipatasertib solubility dmso positive control) for 18 hours at 37°C. Supernatants were collected

as described in Methods. The level of hBD was computed from duplicates of three experiments. Means followed by the same letter are not significantly SSR128129E different. Analysis of hBD2 expression by airway epithelial cells exposed to live A. fumigatus In order to determine if hBD2 expression was induced in the respiratory cells by live A. fumigatus organisms,

RT-PCR and immunofluorescence analysis of cells exposed to unfixed 106 live conidia was performed. Using microscopic observation, we first examined the development of A. fumigatus in the environment of the epithelial A549 or 16HBE cells. When the RC were added to the epithelial cells, they settled onto the cells within 30 minutes and began to swell after 3–4 hours; after 8 hours of infection, the SC became polarised and began to germinate. The germ tubes then progressively elongated, forming the hyphae: after 18 hours of infection, the hyphae had completely covered the epithelial cells (data not shown). RT-PCR analysis of the A549 cells exposed to live A. fumigatus RC for 4, 8 and 18 hours allows us to detect hBD2 expression after 18 hours of incubation (Figure 10A), whereas no inducible hBD2 expression was observed after 4 or 8 hours of incubation (data not shown). Treatment of A549 cells either with IL-1 β or TNF-α for 18 hours resulted in the inducible hBD2 expression. Detection of hBD2 in epithelial cells exposed to live A.

g. [4, 13–16]). This study utilizes an engineering approach, known as robustness analysis, which is used to analyze complex systems. Robustness analysis determines the stability of a system response to perturbations. Robust systems return similar or identical responses when perturbed

while non-robust systems return very different responses [17, 18]. SBE-��-CD concentration biofilm antibiotic tolerance is a product of complex cellular systems. The presented study examines the robustness of colony biofilm antibiotic tolerance to industrially and medically relevant perturbations including 1) nutrient environment 2) temperature 3) quorum sensing ability and 4) growth phase. To our knowledge, this is the first time robustness analysis has been applied to biofilm antibiotic tolerance. Antibiotic tolerance is at the heart of many practical challenges related to unwanted biofilms. Being able to predict biofilm antibiotic tolerance buy LY411575 as a function of culturing perturbations is essential for rationally designing and evaluating antimicrobial strategies. The presented results shed insight on the varying success rates of common

anti-fouling strategies like antibiotic impregnated coatings and provide a template for improved antimicrobial testing schemes. Results 1. Antibiotic tolerance in planktonic and biofilm cultures Biofilms often exhibit very different antibiotic tolerances than planktonic cultures [1–4]. To interpret the presented biofilm data in an appropriate context, the antibiotic tolerances this website of biofilm

cultures were compared to planktonic cultures. Antibiotics representing the aminoglycoside and beta-lactam classes were used as proxies for the diverse array of utilized agents. Kanamycin and ampicillin tolerances were determined for planktonic and Dipeptidyl peptidase biofilm cultures grown in Luria-Bertani (LB) medium at 37°C. These antibiotics were highly effective against planktonic cultures reducing colony forming units (cfu’s)/ml by 6 to 9 orders of magnitude (Fig. 1a). The biofilm antibiotic tolerance results were varied. Kanamycin produced a 9 log10 reduction in cfu’s per biofilm while ampicillin resulted in only a one log10 reduction in cfu’s per biofilm (Fig 1b). Subsequent biofilm responses to culturing perturbations were compared to these base tolerance results (Fig. 1b). Just prior to antibiotic challenge, the biofilm cultures contained 9.3 log10 ± 0.1 cfu’s/biofilm while the planktonic cultures had 7.8 ± 0.2 log10 cfu’s/ml. Additional data illustrating differences in colony biofilm antibiotic susceptibility as compared to planktonic cultures can be found in Additional file 1, Figs. S1 and S5. Figure 1 Comparison of planktonic and biofilm antibiotic tolerance. Wild-type E. coli K-12 cultures were grown on LB only medium at 37°C. Cultures were grown for 6 hours before being transferred to fresh antibiotic treatment medium for 24 hours.