However, meta-analyses have yielded inconsistent conclusions A m

However, meta-analyses have yielded inconsistent conclusions. A meta-analysis of 6 cohort studies and 6 RCTs concluded that current data are not conclusive as to whether statins are protective for CIN [158], while another meta-analysis of data on 1,251 patients from 7 RCTs concluded that periprocedural short-term statin treatment is likely effective in the prevention of CIN [159]. At the present time, we consider not to use statins to prevent CIN. Prevention of contrast-induced nephropathy: dialysis Does hemodialysis conducted after contrast exposure this website as a measure to prevent CIN decrease the risk for

developing CIN? Answer: Because there is no evidence indicating that hemodialysis decreases the risk for developing CIN, we recommend not to use hemodialysis after contrast exposure for this purpose. Is hemofiltration superior to hemodialysis in decreasing the risk for developing CIN? Answer: We consider not to use hemofiltration

as a measure to prevent CIN. Contrast media can be removed from the blood by hemodialysis. It has been reported that 60–90 % of the contrast medium is removed during 1 session of hemodialysis. Clinical studies have been conducted on the basis of these findings to investigate the efficacy of hemodialysis, hemodiafiltration, and hemofiltration in the prevention of CIN [160–169]. However, most studies could not demonstrate the efficacy of these procedures in the prevention of CIN. A few studies have reported a lower risk of CIN, but some others have reported an increased Fostamatinib risk of CIN. The risk of CIN was not changed in a majority of studies. Accordingly, there is no scientific evidence that supports the use of hemodialysis as a measure to prevent CIN. Although studies have been conducted to investigate the efficacy of hemofiltration in preventing CIN, there has been no conclusive evidence that hemofiltration prevents CIN by removing Sinomenine the contrast

medium from the blood. However, in the clinical setting, hemodialysis may be conducted after contrast exposure to prevent heart failure or for other purposes. Treatment of contrast-induced nephropathy Does the treatment of CIN with loop diuretics improve the recovery from AKI? Answer: We recommend not using loop diuretics for the treatment of CIN because it does not improve the recovery from AKI. Most clinical studies on the effects of loop diuretics in the treatment of AKI, including CIN, have concluded that loop diuretics are ineffective in the treatment of AKI [170–174]. In a RCT of 338 patients with AKI requiring dialysis therapy who received either loop diuretics (furosemide) or placebo, furosemide showed no significant improvement for any endpoints tested [173]. In 2 meta-analyses published in 2006 [175] and 2007 [176], loop diuretics were not associated with improved kidney function, rate of hemodialysis, or mortality.

Putting this into a briefing note for researchers can be a helpfu

Putting this into a briefing note for researchers can be a helpful starting point for discussion.  Provide space and resources find more to allow teams and individuals to learn and to build contacts beyond the policy sphere. Table 3 Recommendations aimed at helping organisations improve their science-policy communication Both science and policy  Fund and support interdisciplinary research.  Provide incentives (monetary and career) for interaction between science and policy.  Promote discussions about career structures and motivations.  Fund training or resourcing for “linker/broker/facilitator” individuals and “linker”

events to build science-policy relationships (do not just focus on tangible “knowledge exchange outputs”).  Provide funding for networking events.  Promote general understanding about science and its role in society.  Develop, and regularly revisit, a communication strategy to help identify and prioritise audiences and partners. Science  Research and fund training for communication skills and understanding of policy processes for scientists.  Explore potential for broader assessment of impact (not just journal publications), and create and publish in journals aimed PD-0332991 clinical trial at policy.  Encourage scientists to get acquainted

with policy processes and support those who wish to operate at the science-policy interface.  Provide directories of experts/subject-specific contacts. Policy  Promote transparency and wider understanding (e.g. through training Mirabegron courses) of policy and decision-making and implementation processes.  Explore if and why science is valued compared to other forms of evidence.  Liaise with funders to ensure funded projects (i) are clearly aware of policy priorities, and (ii) encourage communication e.g. enforce clearly written summaries from tender stage.  Liaise with funders to develop projects that allow flexibility for interaction between science and policy. To promote real conversations between science and policy and co-construction of problems and solutions, however, it is not enough to adopt specific piecemeal recommendations. Fundamental changes in science and policy are required, as outlined below. Framing research and policy

jointly Not all research will be directly policy-relevant, and conversely some research will prove unexpectedly relevant. However, for research that aims specifically to answer user needs, framing the problem, research process and solutions jointly with science and policy may improve the likelihood of useful and relevant research outputs. Framing is understood here as “the interpretation process through which people construct and express how they make sense of the world around them” (Gray 2003, p. 12). The interviewees and workshop participants emphasised strongly the need to change how problems are framed and agreed. This is crucial as it influences the way in which research will be carried out and presented, and thus the potential for research outputs to be used in decision-making processes.

Eastern Cooperative Oncology Group N Engl J Med 2000, 343:1217–1

Eastern Cooperative Oncology Group. N Engl J Med 2000, 343:1217–1222.PubMedCrossRef 17. Douillard JY: Adjuvant learn more chemotherapy for non-small-cell lung cancer: it does not always fade with time. J Clin Oncol 28:3–5. 18. Pignon JP, Tribodet H, Scagliotti

GV, Douillard JY, Shepherd FA, Stephens RJ, Dunant A, Torri V, Rosell R, Seymour L, et al.: Lung adjuvant cisplatin evaluation: a pooled analysis by the LACE Collaborative Group. J Clin Oncol 2008, 26:3552–3559.PubMedCrossRef 19. Berghmans T, Paesmans M, Meert AP, Mascaux C, Lothaire P, Lafitte JJ, Sculier JP: Survival improvement in resectable non-small cell lung cancer with (neo)adjuvant chemotherapy: results of a meta-analysis of the literature. Lung Cancer 2005, 49:13–23.PubMedCrossRef 20. Bria E, Gralla RJ, Raftopoulos H, Cuppone F, Milella M, Sperduti I, Carlini

P, Terzoli E, Cognetti F, Giannarelli D: Magnitude of benefit of adjuvant chemotherapy for non-small cell lung cancer: meta-analysis of randomized clinical trials. Lung Cancer 2009, 63:50–57.PubMedCrossRef 21. Hotta K, Matsuo K, Ueoka H, Kiura K, Tabata M, Tanimoto Y-27632 concentration M: Role of adjuvant chemotherapy in patients with resected non-small-cell lung cancer: reappraisal with a meta-analysis of randomized controlled trials. J Clin Oncol 2004, 22:3860–3867.PubMedCrossRef 22. Sedrakyan A, Van Der Meulen J, O’Byrne K, Prendiville J, Hill J, Treasure T: Postoperative chemotherapy for non-small cell lung cancer: A systematic review and meta-analysis. J Thorac Cardiovasc Surg 2004, 128:414–419.PubMedCrossRef 23. Arriagada R, Auperin A, Burdett S, Higgins JP, Johnson DH, Le Chevalier T, Le Pechoux C, Parmar MK, Pignon JP, Souhami RL, et al.: Adjuvant chemotherapy, with or without postoperative radiotherapy, in operable non-small-cell lung cancer: two meta-analyses of individual patient data. Lancet 2010, 375:1267–1277.PubMedCrossRef 24. Banna GL, Di

Maio M, Follador A, Collova E, Menis J, Novello S, Bria E, Airoldi M, Amoroso D, Ardizzoia A, et al.: Italian Survey on adjuvant treatment of non-small cell lung cancer (ISA). Lung Cancer 73:78–88. Inositol monophosphatase 1 25. Booth CM, Shepherd FA, Peng Y, Darling GE, Li G, Kong W, Mackillop WJ: Adoption of adjuvant chemotherapy for non-small-cell lung cancer: a population-based outcomes study. J Clin Oncol 28:3472–3478. 26. Cuffe S, Booth CM, Peng Y, Darling GE, Li G, Kong W, Mackillop WJ, Shepherd FA: Adoption of adjuvant chemotherapy (ACT) for non-small cell lung cancer (NSCLC) in the elderly: A population-based outcomes study. ASCO Meeting Abstracts 29:7012. 27. Gu F, Strauss GM, Wisnivesky JP: Platinum-based adjuvant chemotherapy (ACT) in elderly patients with non-small cell lung cancer (NSCLC) in the SEER-Medicare database: Comparison between carboplatin- and cisplatin-based regimens. ASCO Meeting Abstracts 29:7014. 28.

Results and discussion Figure  1 shows the emission currents of t

Results and discussion Figure  1 shows the emission currents of the CNTs, which are listed in Table  1, as a function of the applied voltage. The electron emission characteristics of the deposited CNTs were measured using a compactly designed field emission measurement system. The distance between the cathode (CNT) and the anode (ITO-coated glass) was carefully adjusted to be kept at 1 mm by using a micro-spacing control system. It is clearly seen in Figure  1 that the thermally treated CNTs

(i.e., CNT-B and CNT-D) revealed much better emission characteristics than those of the as-deposited CNTs (i.e., CNT-A and CNT-C), while selleck kinase inhibitor the coating of Al interlayer seems to hardly affect the emission characteristics. p38 MAPK inhibitors clinical trials From the emission characteristics, the maximum emission current (I max, μm) and turn-on voltage (V on, V) of the CNTs were estimated by defining the I max as the emission current measured at the applied voltage of 1.2 kV and the I on as the voltage applied to obtain the emission current of 10 μA. Also, the field enhancement factor (β) values of the CNTs were calculated by applying the emission current characteristics of Figure  1 to the Fowler-Nordheim theory with the work function of CNTs to

be 5.0 eV [16]. The values of I max, V on, and β estimated from all of the CNTs are summarized in Table  1. The results showed that the drastic increase of I max and the decrease of V on were induced by the thermal treatment of CNTs, regardless of any Al interlayer coating. The β values, on the other hand, were not much different from CNT-A to CNT-D and estimated to be within the range from 4.30 × 104 to 4.98 × 104. Figure 1 The emission current versus electric field characteristics of CNTs. The inserted

photos represent the FESEM images of the exterior shapes and CNTs’ surfaces for the samples CNT-A and CNT-C. For all of the CNTs, the changes in the surface morphologies due to thermal treatment and Al interlayer coating were monitored by using a field emission scanning electron microscope (FESEM; JSM-6330 F, JEOL, Tokyo, Japan). The FESEM images Dichloromethane dehalogenase of the exterior shapes and the enlarged surfaces for the CNT-A (without Al interlayer) and CNT-C (with Al interlayer) emitters are compared in Figure  1. It seemed that no significant differences in their surface morphologies were observed. It was also observed in this study that thermal treatment hardly affected the surface morphologies of the CNTs, although their FESEM images are not displayed in Figure  1. This may indicate that neither the coating of Al interlayer nor the thermal treatment altered the structural aspect ratios of the CNTs. Also, this may be in good agreement with the results that the β values were similar for all of the CNTs. To discover any other reason that can account for the results shown in Figure  1, the microstructures of the CNTs were analyzed via Raman spectroscopy (T64000, Jobin Yvon, Edison, NJ, USA).

Arch Surg 1993, 128:765–770 PubMedCrossRef 30 Schraufnagel D, Ra

Arch Surg 1993, 128:765–770.PubMedCrossRef 30. Schraufnagel D, Rajaee S, Millham FH: How many sunsets?Timing of surgery in adhesive small bowel obstruction: A study of the Nationwide Inpatient Sample. J Trauma Acute Care Surg 2013,74(1):181–187. doi:10.1097/TA.0b013e31827891a1 . discussion 187–9PubMedCrossRef

31. Diaz JJ Jr, Bokhari F, Mowery NT, Acosta JA, Block EF, Bromberg WJ, Collier BR, Cullinane DC, Dwyer KM, Griffen MM, Mayberry JC, Jerome R: Guidelines for management of small bowel obstruction. J Trauma 2008,64(6):1651–1664.PubMedCrossRef 32. Guo S-B, Duan Z-J: Decompression of the small bowel by endoscopic long-tube SRT1720 manufacturer placement. World J Gastroenterol 2012,18(15):1822–1826. doi:10.3748/wjg.v18.i15.1822PubMedCrossRef 33. Assalia MLN2238 mouse A, Kopelman D, Bahous H, Klein Y, Hashmonai M: Gastrografin for mechanical partial, small bowel obstruction due to adhesions. Harefuah 1997,132(9):629–633.PubMed 34. Choi HK, Law WL, Ho JW, Chu KW: Value of gastrografin in adhesive small bowel obstruction after unsuccessful conservative treatment: a prospective evaluation. World J Gastroenterol 2005,11(24):3742–3745.PubMed 35. Burge J, Abbas SM, Roadley G, Donald J, Connolly A, Bissett IP, Hill AG: Randomized controlled trial of Gastrografin in adhesive small bowel obstruction. ANZ J Surg 2005,75(8):672–674.PubMedCrossRef 36. Wadani HAI, Awad NIA, Hassan KA, Zakaria HM, Abdulmohsen

Al Mulhim A, Alaqeel FO: Role of water soluble contrast agents in assigning patients to a Non-operative course in adhesive small bowel obstruction.

Oman Medical Journal 2011,26(6):454–456. doi:10.5001/omj2011.116PubMedCrossRef 37. Biondo S, Parés D, Mora L, Martí Ragué J, Kreisler E, Jaurrieta E: Randomized clinical study of Gastrografin administration Grape seed extract in patients with adhesive small bowel obstruction. J Surg 2003,90(5):542–546. 38. Abbas SM, Bissett IP, Parry BR: Meta-analysis of oral water-soluble contrast agent in the management of adhesive small bowel obstruction. Br J Surg 2007,94(4):404–411.PubMedCrossRef 39. Chen SC, Yen ZS, Lee CC, Liu YP, Chen WJ, Lai HS, Lin FY, Chen WJ: Nonsurgical management of partial adhesive small-bowel obstruction with oral therapy: a randomized controlled trial. CMAJ 2005,173(10):1165–1169.PubMedCrossRef 40. Ambiru S, Furuyama N, Kimura F, Shimizu H, Yoshidome H, Miyazaki M, Ochiai T: Effect of hyperbaric oxygen therapy on patients with adhesive intestinal obstruction associated with abdominal surgery who have failed to respond to more than 7 days of conservative treatment. Hepatogastroenterology 2008,55(82–83):491–495.PubMed 41. Cox MR, Gunn IF, Eastman MC, Hunt RF, Heinz AW: The safety and duration of non-operative treatment for adhesive small bowel obstruction. Aust N Z J Surg 1993,63(5):367–371.PubMedCrossRef 42. Shou-Chuan S, Kuo-Shyang J, Lin S-C, et al.

0 and pH 5 5, which was also found in strain SA45 The same expre

0 and pH 5.5, which was also found in strain SA45. The same expression pattern has been found for the prophage-encoded Panton-Valentine leukocidin (PVL, luk-PV) of S. aureus [28]. Maximal expression of luk-PV in the late exponential growth phase was followed by a rapid decline post-exponentially. Our observation could partially be explained by the induction of the prophage carrying the toxin gene. The sea-phage copy numbers of S. aureus Mu50 at pH 6.0 remained constant during the first part of cultivation. In the late stationary growth phase, however,

the number had increased four times (average R788 increase of two biological replicates) compared to levels in early stationary growth phase. The phage copy numbers might have increased further if growth was allowed to continue. An acetic-acid induced intracellular drop in pH, leading to oxidative stress [29] would activate the SOS response system inducing the prophage [30]. Sumby and Waldor showed that upon prophage induction in S. aureus, the phage DNA was replicated, resulting in an increase in sea gene copy number, and that a second prophage-regulated sea promoter was also activated, resulting in increased sea expression [14]. Similar enhanced transcription

of phage-encoded virulence genes upon prophage induction has also been observed for PVL in S. aureus and the Shiga toxins in E. coli [28, 31]. Mitomycin C, a well-known GSK 3 inhibitor prophage inducer, was used in this study. The more MC added, the more SEA was produced per CFU for all three strains tested, supporting

the association between prophage induction and SEA production. However, the expected boost in extracellular SEA levels accompanying the increased sea mRNA levels and sea gene copy levels observed at pH 5.5 was not found. This could be because of the pronounced phage production at pH 5.5 seen as a rapid increase in extracellular sea-phage copy number (Figure 3). The window for phage-encoded SEA-biosynthesis prior to phage-release could be too narrow in the bacteria at this pH level. The relative phage copy number generally increased over time at all pH levels investigated. At pH 5.5, the relative phage copy number was increasing dramatically over time, suggesting that substantial prophage induction had occurred. The sea gene copy number, however, was decreasing over Ureohydrolase time at pH 5.5. This could be due to cell lysis occurring upon prophage induction at this pH. At pH 5.0 and 4.5, a big increase in relative sea gene copy number was observed between the two last sampling points. This suggests that the prophage has been induced and the replicative form of the phage DNA is produced. However, at these low pH values, no great increase in SEA or phage copies were observed, suggesting protein synthesis was impaired. In addition, the reason why the sea expression of S. aureus Mu50 at pH 5.5 was not as high as at pH 6.

[29] These two types of BEs with different surface roughness wer

[29]. These two types of BEs with different surface roughness were prepared by controlling the deposition method (sputtering or PECVD) and parameters such as power or working pressure during sputtering. The

AFM images of smooth and nanotip BE surfaces are shown in Figure  5. Figure  5a,c shows two-dimensional (2D) or planeviews of surface roughness for the smooth and nanotip samples, respectively. Figure  5b,d shows 3D views of the smooth and nanotip samples, respectively. The average (R a) and root mean square (rms; R q) surface roughness values of smooth and nanotip BE surfaces are found to be 1.05 and 1.35 nm, and 3.35 and 4.21 nm, respectively. These self-assembled nanotips are Ensartinib price observed from our W BE surface. Experimental data shows

that the switching cycle uniformity and pulse endurance were greatly improved in the devices with nanotip BE surface. This is due to the controlled and easy formation/rupture of the conducting filament during switching owing to the enhanced electric field at the nanotips observed in the AFM image. Also, it is expected that the film will be more defective on the nanotip BE surface. Due to these reasons, the cross-point memory device shows almost forming-free or low-voltage operation. Figure  6 shows the device-to-device cumulative probability plot of LRS and HRS of cross-point memory devices with different sizes of 4 × 4, 20 × 20, and CHIR-99021 in vitro 50 × 50 μm2, respectively. More than 20 cross-points of each size have been measured randomly across the 4-in. wafer. Most of the devices show click here resistive switching with an HRS/LRS ratio of >10. The average resistance of LRS increases by decreasing the device size from 50 × 50 to 4 × 4 μm2. This might be due to

the multifilament formation which is more probable when the device size is large, which is due to the nonuniform deposition of the switching layer on the sidewalls. It is expected that device-to-device uniformity can further be improved under a better facility. In order to confirm the nonvolatility of LRS and HRS, the resistance of both states is monitored with time and plotted in Figure  7a. The read voltage was +0.2 V. As can be seen, both LRS and HRS are fairly stable for more than 104 s at room temperature. Figure  7b shows the ac endurance capability of our cross-point memory device. The device was successively programmed and erased at +2.5/−2.5 V with 500-μs pulse, respectively, and read after each program/erase event at +0.2 V, as schematically shown inside Figure  7b. The data of every such program/erase event is recorded and plotted. The read pulse width was 10 ms. Due to every cycle read, variation of HRS/LRS with cycle-to-cycle is observed, which is slight read disturb. Further study is necessary to overcome this problem. However, an excellent ac endurance of more than 105 cycles is achieved.

coli has revealed a strong correlation between the presence of th

coli has revealed a strong correlation between the presence of the yfeABCD operon and virulence [35]. In this study we have shown that the yfeABCD Selleck Inhibitor Library operon is important for the virulence of P. luminescens is some insect hosts. Therefore the Δyfe mutant was as virulent as the WT bacteria in one lepidopteran insect host, G. mellonella, but

was completely avirulent in another lepidopteran host, M. sexta. This implicates the yfeABCD operon as a possible host-range determining locus in P. luminescens. The defect in virulence observed with the Δyfe mutant was rescued by the pre-loading the insect with Fe3+ but not Mn2+ suggesting that the role of the Yfe transporter in insect virulence is associated with iron homeostasis (data not shown). In this

study we have also shown that the Yfe transporter may have a role during the symbiotic interaction with the nematode, in particular during the colonization of the IJ. We observed that the Δyfe mutant has a very low plating efficiency, compared to WT, on LB agar when isolated directly from the IJ nematode. This low learn more plating efficiency was rescued by the addition of either pyruvate or catalase, known scavengers of H2O2, to the LB agar plates. Therefore the Δyfe mutant appears more sensitive to H2O2 than the WT bacteria. The Yfe transporter can mediate the uptake of Mn2+ and it has been shown that Mn2+ can protect the cells from ROS [18, 22]. Although it was thought that part of this protective affect was due to the ability of Mn2+ to act as a chemical scavenger of ROS, recent evidence suggests that the role of Exoribonuclease Mn2+ during oxidative stress in E. coli is as an enzyme co-factor (i.e. replacing the Fe2+ in Fe-S clusters that are sensitive to oxidative stress) [25]. Many bacteria contain a dedicated

Nramp-like Mn2+ transporter called MntH [18, 37]. In E. coli the expression of mntH can be induced by oxidative stress and it has been reported that mntH yfe double mutants in Salmonella, APEC and Shigella are sensitive to H2O2 [38–40]. Therefore Mn2+ uptake appears to be critical in some cells for their ability to survive exposure to H2O2. Interestingly analysis of the Pl TT01 genome reveals that there is no mntH homologue in Pl TT01 and, therefore, the Yfe transporter is the only means by which Pl TT01 is predicted to be able to obtain Mn2+ from the environment. However we could not detect any inherent increase in the sensitivity of the Δyfe mutant to H2O2 during growth on LB agar plates. This suggests that there is something specific about the conditions within the nematode that induces the H2O2-sensitive phenotype in Pl TT01 Δyfe. Recent studies in the model nematode Caenorhabditis elegans (a close relative of Heterorhabditis) have shown that this nematode produces 3 intestinally localized Nramp-like proteins that are involved in Mn2+ transport from the gut lumen [41, 42]. Therefore, the levels of Mn2+ available to Pl TT01 within the gut of the IJ are likely to be very low.

The observation of a current-independent point in ρ xx which corr

The observation of a current-independent point in ρ xx which corresponds to its temperature-independent counterpart suggests that applying a high current is equivalent check details to heating up the graphene lattice. Conclusions In conclusion,

we have presented magnetoresistivity measurements on multilayer epitaxial graphene. It is found that a relation between the effective Dirac fermion temperature and the driving current can be given by T DF ∝ I ≈0.5 in the low magnetic field regime. With increasing magnetic field, an I-independent point in ρ xx is observed which is equivalent to its T-independent counterpart in the low current limit. Evidence for direct I-QH transition has been reported in four different graphene samples. Near the crossing field where the longitudinal resistivity is approximately T-independent, ρ xx is at least two times larger than ρ xy. Moreover, the product of Drude mobility and B c is smaller than 1. We suggest that further studies are required to obtain a complete understanding of direct I-QH transition in disordered graphene. Acknowledgements This work was funded by the National Science Council (NSC), Taiwan and National Taiwan University

(grant number 102R7552-2). Electronic supplementary material Additional file 1: Figure S1: The magnetoresistivity measurements ρ xx (B) at different T for sample 2. The inset shows the Hall measurements ρ xy (B) at different T for sample 2. Figure S2 The magnetoresistivity measurements ρ xx (B) at different T for sample 3. The inset shows the Hall measurements ρ xy (B) at different T for sample 3. Figure S3 The magnetoresistivity measurements ρ xx (B) at different T for sample Pexidartinib ic50 4. The inset

shows the Hall measurements ρ xy (B) at different T for sample 4. (DOCX 3 MB) References 1. Novoselov KS, Geim AK, Morozov SV, Jiang D, Zhang Y, Dubonos SV, Grigorieva IV, Firsov AA: Electric field effect in atomically thin carbon films. Science 2004, 306:666.CrossRef 2. Zhang Y, Tan Y-W, Stormer HL, Kim P: Experimental observation of the quantum Hall effect and Berry’s phase in graphene. Nature 2005, 438:201.CrossRef 3. Novoselov KS, Geim AK, Morozov SV, Jiang D, Katsnelson MI, Grigorieva IV, Dubonos SV, Firsov AA: Dichloromethane dehalogenase Two-dimensional gas of massless Dirac fermions in graphene. Nature 2005, 438:197.CrossRef 4. Bolotin KI, Ghahari F, Shulman MD, Stormer HL, Kim P: Observation of the fractional quantum Hall effect in graphene. Nature 2009, 462:196.CrossRef 5. Du X, Skachko I, Duerr F, Luican A, Andrei EY: Fractional quantum Hall effect and insulating phase of Dirac electrons in graphene. Nature 2009, 462:192.CrossRef 6. Feldman BE, Krauss B, Smet JH, Yacoby A: Unconventional sequence of fractional quantum Hall states in suspended graphene. Science 2012, 337:1196.CrossRef 7. Lin Y-M, Valdes-Garcia A, Han S-J, Farmer DB, Meric I, Sun Y, Wu Y, Dimitrakopoulos C, Grill A, Avouris P, Jenkins KA: Wafer-scale graphene integrated circuit. Science 2011, 332:1294.CrossRef 8.

Infect Immun 1996,64(9):3811–3817 PubMed 34 Hentges DJ, Que JU,

Infect Immun 1996,64(9):3811–3817.PubMed 34. Hentges DJ, Que JU, Casey SW, Stein AJ: The influence of streptomycin on colonization resistance in mice. Microecol Theor 1984, 14:53–62. Competing interests The authors declare that they have no competing interests. Authors’ contributions EJB participated in the study design, carried

out laboratory work, analysed the data, and drafted the manuscript. LNN participated in the study design, carried out laboratory work, analysed the data, and edited the manuscript. KAK Small molecule library participated in the study design, edited the manuscript, and received the funding needed to complete the research. CS conceived the study, carried out laboratory work, analysed the data, and edited the manuscript. All authors have read and approved the final manuscript.”
“Background Pockmarks, described as craterlike depressions on the seafloor, were first discovered at the Scotian Shelf and are likely to be formed by ascending gas or water [1]. The features have later been discovered throughout the world’s oceans, e.g. the Norwegian continental slope [2], the equatorial West African margin [3], the Bering Sea [4] and the Belfast Bay, Maine [5]. Pockmarks may in some instances be related to active seepage, such as at Gullfaks and Tommeliten (North Sea), Imatinib mouse where methane is emitted at the seafloor.

At these sites anaerobic methanotrophic archaea (ANME) have been found to be important members of the microbial community in the sediments [6, 7]. ANME and Molecular motor their sulphate reducing bacterial partners are key players in anaerobic methane oxidation and ubiquitous in all methane environments (e.g. Haakon Mosby Mud Volcano [8], Coal Oil Point seep sediments

[9], Eel River sediments [10], Black Sea microbial mats and Hydrate Ridge [11]) [12]. One area characterized by a high density of pockmarks is the seabed overlaying the Troll petroleum reservoir in the North Sea [13]. The pockmarks in this area have diameters up to about 250 m and depths up to around 10 m below the surrounding seafloor level [13, 14]. The Troll pockmarks were most likely formed by expulsion of methane from decomposing methane hydrates, caused by increasing temperatures at the end of the last glaciation period about 11000 years ago [15]. No free gas has been detected in shallow sediments of the area at the present time; increasing concentrations of dissolved methane with depth have however been measured from approximately 70 m below seafloor (bsf) [15]. Although sporadic gas bubbles may still be emitted, it is believed that the main force keeping these pockmarks from being filled by sediments is the water-current activity in the craters and porewater flux [15, 16]. The Troll field is one of the largest accumulations of petroleum discovered in the North Sea [17]. The reservoir consists of sandstones from the Late Jurassic Sognefjord Formation and is located between 1000 and 1300 m bsf [18].