Blood 2005, 105:1950–1955.PubMedCrossRef 43. Wittchen ES, Worthylake RA, Kelly P, Casey PJ, Quilliam LA, Burridge K: Rap1 GTPase inhibits leukocyte transmigration by promoting endothelial barrier function. J Biol Chem 2005, 280:11675–11682.PubMedCrossRef 44. Birukova AA, Zagranichnaya T, Alekseeva E, Bokoch GM, Birukov KG: Epac/Rap and PKA are novel mechanisms of ANP-induced Rac-mediated pulmonary endothelial Seliciclib cell line barrier protection. J Cell Physiol 2008, 215:715–724.PubMedCrossRef

45. Gong P, Angelini DJ, Yang S, Xia G, Cross AS, Mann D, et al.: TLR4 signaling is coupled to SRC family kinase activation, tyrosine phosphorylation of zonula adherens proteins, and opening of the paracellular pathway in human lung microvascular endothelia. J Biol Chem 2008, 283:13437–13449.PubMedCrossRef 46. Sakarya S, Rifat S, Zhou J, Bannerman DD, Stamatos NM, Cross AS, et al.: Mobilization of neutrophil sialidase activity desialylates the pulmonary vascular endothelial surface and increases resting neutrophil adhesion to and migration across the endothelium. Glycobiology 2004, 14:481–494.PubMedCrossRef 47. Goldblum SE, Van Epps DE, Reed WP: Serum inhibitor of C5 fragment-mediated polymorphonuclear leukocyte chemotaxis associated with chronic hemodialysis.

J Clin Invest 1979, 64:255–264.PubMedCrossRef 48. Sun selleckchem L, Vitolo M, Passaniti A: Runt-related gene 2 in endothelial cells: inducible expression and specific regulation of cell migration and invasion. Cancer Res 2001, 61:4994–5001.PubMed 49. Matyakhina L, Lenherr SM, Stratakis CA: Protein kinase A and chromosomal stability. Ann N Y Acad Sci 2002, 968:148–157.PubMedCrossRef 50. Angelini DJ, Hyun SW, Grigoryev DN, Mephenoxalone Garg P, Gong P, Singh IS, et al.: TNF-alpha increases tyrosine phosphorylation of vascular endothelial cadherin and

opens the paracellular pathway through fyn activation in human lung endothelia. Am J Physiol Lung Cell Mol Physiol 2006, 291:L1232-L1245.PubMedCrossRef Authors’ contributions CN was responsible for acquisition of data and writing the manuscript. CF assisted in the isolation of neutrophils, participated in the design of the study and assisted in drafting the manuscript. MZ performed the statistical analysis. AC participated in study design, drafting the manuscript, and revising it critically. SG participated in study design, drafting the manuscript, and revising it critically. All authors read and approved the final manuscript.”
“Background Enteric methane emitted by livestock species is produced by symbiotic methanogens which use as substrates the CO2 and H2 that result from digestion of plant fibers in the gastrointestinal tract of their host. Because it is not assimilated, methane is released into the environment, mostly through eructation [1].

Paclitaxel induces formation of excess disordered microtubules by promoting microtubule polymerization and stability. Since paclitaxel inhibits depolymerization of microtubules,[2,3] cell division is inhibited. Thus, paclitaxel has antitumor activity. Paclitaxel is used clinically in the treatment of ovarian, breast, endometrial, stomach, and non-small cell lung cancers in Japan. The main adverse drug reactions to paclitaxel include

gastrointestinal Fostamatinib supplier symptoms, peripheral neuropathy, arthralgia, muscular pain, nausea and vomiting, epilation, and pyrexia. Paclitaxel tends to be soluble in N,N-dimethylacetamide, acetonitrile, methanol, and ethanol but is relatively insoluble in water. Because 50% ethanol is used as the solvent for clinical mTOR inhibitor paclitaxel injections,[4] we hypothesized that impairment of specific central nervous system (CNS) functions by ethanol or its cleavage product, acetaldehyde, as well as adverse reactions related to intoxication, may occur following treatment with this preparation. Thus, the possibility of adverse reactions following intake of ethanol accompanying paclitaxel administration should not be overlooked. Since many hospitals in Japan are located in rural areas and are not conveniently accessible by public transportation, most patients drive to the hospital. Thus, it is important to consider the possible

CNS depressant actions Baricitinib of ethanol contained in injectable drug formulations, in order to reduce the risk of serious car accidents. Furthermore, in the Road Traffic Act in Japan, the breath ethanol concentration

that constitutes drunk driving is 0.15 mg/L[5] This threshold is lower than those in the UK, USA, and Canada (0.40 mg/L), and those in Australia, Germany, and France (0.25 mg/L). It is important to ensure that patients who receive paclitaxel injections containing ethanol do not have breath ethanol concentrations exceeding the legal threshold. Although research on plasma ethanol concentrations following paclitaxel administration has been published previously,[6] only a few reports have evaluated the correlation between ethanol intake during chemotherapy and the ethanol concentration in exhaled breath. Here, we investigated the concentration of ethanol in exhaled breath after chemotherapy with an intravenous paclitaxel infusion. Methods Patients Thirty Japanese outpatients (mean age 55 ± 8.6 years [range 35–74]; 2 male and 28 female) who received treatment with paclitaxel (80–330 mg/day) for breast, ovarian, or gastric cancer were eligible subjects for this research. This clinical study was approved by the Institutional Review Board for Clinical Trials at Gunma University Hospital (Maebashi, Japan). Written consent was obtained from all patients after they were informed of the study procedure.

33WO3 nanoparticle found in related records (PDF 01-081-1244), and V cell was used as 0.361 nm3[19]. Figure 3 XRD patterns and SEM images. XRD patterns (a) and SEM images of as-prepared Cs0.33WO3 before (b) and after (c) the stepwise bead milling process Bortezomib concentration for randomly shaped nanoparticles. The LSPR is reportedly influenced

by the morphology. In tungsten oxide, however, its effect on the NIR absorption characteristics is minor [7]. To consider the randomly shaped nanoparticles fabricated through a solid reaction, depolarization factors were also used as indicated in Equation 7, which assumes an aspect ratio-related factor (S) of 0.417. (7) Incident light reflection by the difference in refractive indices between the layers The incident light passing through the coated film is interrupted due to differences in the light velocity caused by differences in the interlayer

refractive index. In a double layer-coated film, this interruption occurs between the layers of different materials (the tungsten bronze-coated layer (1) and the PET substrate (2)), which partially reflect the incident light. As stated in Equation 8, the contribution for the interlayer reflection (T multilayer) has been considered. (8) in which r 1 and r 2 are the refractive Silmitasertib manufacturer indices of the coated layer and PET substrate, respectively, while θ′ refers to the phase thickness of the coated layer. The reflectance can be calculated using the refractive indices of the coated layer (n 1) and PET substrate (n 2) as stated in Equations 9, 10, and 11. (9) (10) (11) Incident light scattering

according to the size of the nanoparticles Figure 3 reveals the mean diameter of Cs0.33WO3 nanoparticles, which was determined using the image J obtained through TEM and SEM measurements. In a top-down synthesis via the grinding method, the particle sizes are broadly distributed. In these particles, Rayleigh scattering (T scattering) occurs as indicated in Equation 12: (12) in which θ is the scattering angle assumed to be 90°, while n and d are the refractive indices of the nanoparticle. The term R refers to the internanoparticle distance and was calculated using Equation 13 that considers the volume of nanoparticle (V Dolichyl-phosphate-mannose-protein mannosyltransferase p) and the residual weight (TGA (g)) as measured via thermogravimetric analysis (TGA). (13) The total light transmission and shielding functions for the tungsten bronze film The total LTS characteristics have been measured using the absorbance of the transparent near-infrared absorption film from the visible to the infrared regions. In addition, the calculated value is typically slightly below the measured value due to specimen nonuniformity and plasmon damping caused by surface electron scattering [20]. To consider this type of damping, the results were calibrated via numerical analysis. However, the hard-to-measure electrical conductivity of the nanoparticle was set at 1.03 × 10−8 Ω−1 cm−1.

PubMedCrossRef 17. Makino K, Oshima K, Kurokawa K, Yokoyama K, Uda T, Tagomori

K, Iijima Y, Najima M, Nakano M, Yamashita A, et al.: Genome sequence of Vibrio parahaemolyticus : a pathogenic mechanism distinct from that of V cholerae . Lancet 2003,361(9359):743–749.PubMedCrossRef 18. Johnson JA, Panigrahi P, Morris JG Jr: Non-O1 Vibrio cholerae NRT36S produces a polysaccharide capsule that determines colony morphology, serum resistance, and virulence in mice. Infect Immun 1992,60(3):864–869.PubMed 19. Wright AC, Powell JL, Kaper JB, Morris JG Jr: Identification of a group 1-like capsular polysaccharide operon for Vibrio vulnificus . Infect Immun 2001,69(11):6893–6901.PubMedCrossRef 20. Stroeher UH, Manning PA: Genetics of Vibrio cholerae O1 and O139 surface polysaccharides. Boca Raton, Fl.: CRC Press; 1999. 21. Stroeher UH, Parasivam G, Dredge BK, Manning PA: Novel Vibrio cholerae O139 genes involved selleck compound in lipopolysaccharide biosynthesis. J Bacteriol 1997,179(8):2740–2747.PubMed 22. Ali A, Rashid MH, Karaolis DK: High-frequency rugose exopolysaccharide production by Vibrio cholerae . Appl Environ Microbiol 2002,68(11):5773–5778.PubMedCrossRef

23. Xu M, Yamamoto K, Honda T, Ming X: Construction and characterization of an isogenic mutant of Vibrio parahaemolyticus having a deletion in the thermostable direct hemolysin-related hemolysin gene (trh). J Bacteriol 1994,176(15):4757–4760.PubMed 24. Wang H, Griffiths MW: Mg2+-free buffer elevates transformation efficiency of Vibrio parahaemolyticus by electroporation. Lett Appl Microbiol 2009,48(3):349–354.PubMedCrossRef 25. Hamashima H, Iwasaki M, Arai T: A simple and rapid method Selleckchem INK128 for transformation of Vibrio species by electroporation. Methods Mol Biol 1995, 47:155–160.PubMed 26. Meibom KL, Blokesch M, Dolganov NA, Wu CY, Schoolnik GK: Chitin induces natural

competence in Vibrio cholerae . Science 2005,310(5755):1824–1827.PubMedCrossRef 27. Gulig PA, Tucker MS, Thiaville PC, Joseph JL, Brown RN: USERTM friendly cloning coupled with chitin-based natural transformation enables rapid mutagenesis of Vibrio vulnificus . Appl Environ Microbiol 2009,75(15):4936–49.PubMedCrossRef Obatoclax Mesylate (GX15-070) 28. Whitfield C: Biosynthesis and assembly of capsular polysaccharides in Escherichia coli . Annu Rev Biochem 2006, 75:39–68.PubMedCrossRef 29. Chun J, Grim CJ, Hasan NA, Lee JH, Choi SY, Haley BJ, Taviani E, Jeon YS, Kim DW, Lee JH, et al.: Comparative genomics reveals mechanism for short-term and long-term clonal transitions in pandemic Vibrio cholerae . Proc Natl Acad Sci USA 2009,106(36):15442–15447.PubMedCrossRef 30. Iguchi T, Kondo S, Hisatsune K: Vibrio parahaemolyticus O serotypes from O1 to O13 all produce R-type lipopolysaccharide: SDS-PAGE and compositional sugar analysis. FEMS Microbiol Lett 1995,130(2–3):287–292.PubMedCrossRef 31. Datsenko KA, Wanner BL: One-step inactivation of chromosomal genes in Escherichia coli K-12 using PCR products. Proc Natl Acad Sci USA 2000,97(12):6640–6645.PubMedCrossRef 32.

Hadingham KL, Wingrove P, Le Bourdelles B, Palmer KJ, Ragan CI, Whiting PJ. Cloning of cDNA sequences encoding human alpha 2 and alpha 3 gamma-aminobutyric acid A receptor subunits and characterization of the benzodiazepine pharmacology of recombinant alpha 1-, alpha 2-, alpha 3-, and alpha 5-containing human gamma-aminobutyric acid A receptors. Mol

Pharmacol. 1993;43:970–5.PubMed 25. Watanabe Y, Shibuya T, Khatami S, Salafsky B. Comparison of typical and atypical benzodiazepines on the central and peripheral benzodiazepine receptors. Jpn J Pharmacol. 1986;42:189–97.PubMedCrossRef 26. Greenblatt DJ, Harmatz JS, von Moltke LL, Wright CE, Durol AL, Harrel-Joseph LM, Shader RI. Comparative kinetics and response to the benzodiazepine agonists triazolam and zolpidem: evaluation of sex-dependent differences. J Pharmacol Exp Ther. 2000;293:435–43.PubMed 27. Greenblatt DJ, XL765 nmr Harmatz JS, von Moltke LL, Ehrenberg BL, Harrel L, Corbett K, Counihan M, Graf JA, Darwish M, Mertzanis P, Martin PT, Cevallos WH, Shader RI. Comparative kinetics and dynamics of zaleplon, zolpidem, and placebo. Clin Pharmacol Ther. 1998;64:553–61.PubMedCrossRef 28. Gustavson LE, Carrigan PJ. The clinical pharmacokinetics of single doses

of estazolam. Am J Med. 1990;88:2S–5S.PubMedCrossRef 29. Saari TI, Laine K, Leino K, Valtonen M, Neuvonen PJ, Olkkola KT. Effect of voriconazole on the pharmacokinetics and pharmacodynamics of zolpidem GDC-0068 in vivo in healthy subjects. Br J Clin Pharmacol. 2007;63:116–20.PubMedCrossRef 30. Olubodun JO, Ochs HR, von Moltke LL, Roubenoff R, Hesse LM, Harmatz JS, Shader RI, Greenblatt DJ. Pharmacokinetic properties of zolpidem in elderly and young

adults: possible modulation by testosterone in men. Br J Clin Pharmacol. 2003;56:297–304.PubMedCrossRef 31. Tornio A, Neuvonen PJ, Backman JT. The CYP2C8 inhibitor gemfibrozil does not increase the plasma concentrations of zopiclone. Eur J Clin Pharmacol. 2006;62:645–51.PubMedCrossRef L-NAME HCl 32. Nakajima T, Takazawa S, Hayashida S, Nakagome K, Sasaki T, Kanno O. Effects of zolpidem and zopiclone on cognitive and attentional function in young healthy volunteers: an event-related potential study. Psychiatry Clin Neurosci. 2000;54:37–40.PubMedCrossRef 33. Villikka K, Kivistö KT, Lamberg TS, Kantola T, Neuvonen PJ. Concentrations and effects of zopiclone are greatly reduced by rifampicin. Br J Clin Pharmacol. 1997;43:471–4.PubMedCrossRef 34. Tokairin T, Fukasawa T, Yasui-Furukori N, Aoshima T, Suzuki A, Inoue Y, Tateishi T, Otani K. Inhibition of the metabolism of brotizolam by erythromycin in humans: in vivo evidence for the involvement of CYP3A4 in brotizolam metabolism. Br J Clin Pharmacol. 2005;60:172–5.PubMedCrossRef 35. Osanai T, Ohkubo T, Yasui N, Kondo T, Kaneko S. Effect of itraconazole on the pharmacokinetics and pharmacodynamics of a single oral dose of brotizolam. Br J Clin Pharmacol. 2004;58:476–81.PubMedCrossRef 36.

All treatments were carried out for 18 h in a 5% CO2 atmosphere. Determination of macrophage viability Following treatments with either the recombinant SspA or bacterial cells, cell viability was evaluated with an MTT (3-[4,5-diethylthiazol-2-yl]-2,5-diphenyltetrazolium bromide) test performed according to the manufacturer’s protocol (Roche Diagnostics, Mannheim, Germany). Determination of cytokine secretion Commercial enzyme-linked immunosorbent assay (ELISA) kits (R&D Systems, Minneapolis, MN, USA) were used to quantify IL-1β, IL-6, TNF-α, CCL5, and CXCL8 concentrations in the cell-free culture supernatants according to the manufacturer’s protocols. The

absorbance at 450 nm was read using a microplate reader with the wavelength correction set at 550 nm. The rated sensitivities of the commercial ELISA kits were 3.9 pg/ml for IL-1β, 9.3 pg/ml for IL-6, 15.6 MI-503 in vitro pg/ml for TNF-α and CCL5, and 31.2 pg/ml for CXCL8. Determination of cytokine degradation Degradation of IL-6, CXCL8, and CCL5 by the recombinant

SspA was assessed by ELISA. Briefly, recombinant cytokines (300 pg/ml of IL-6, selleck kinase inhibitor 250 pg/ml of CXCL8, or 500 pg/ml of CCL5,) were incubated with the recombinant SspA at concentrations ranging from 0.26 to 16.5 μg/ml for 4 h. Following incubation, residual cytokines were quantified by ELISA as described above. Effect of kinase inhibitors on cytokine secretion Specific kinase inhibitors (Calbiochem, Mississauga, ON, Canada) used at the optimal concentration recommended by the manufacturer (0.0625 μM) were added to macrophages those 2 h prior to being treated with the recombinant SspA (0.33 μg/ml) for 18 h. The inhibitors SB203580 [p38 mitogen-activated kinase (p38MAPK) inhibitor], UO126 [mitogen-activated extracellular kinase 1, 2 (MEK 1, 2) inhibitor] and JNK inhibitor II [c-JUN N-terminal kinase (JNK) inhibitor], were evaluated for their effect on IL-6, CXCL8, and CCL5 secretion by macrophages.

Statistical analysis All treatments and cytokine determination were performed in triplicate and the means ± standard derivations were calculated. Differences were analyzed for statistical significance using the Student’s t-test and were considered significant at P < 0.01. Results Prior to determine the capacity of the recombinant SspA of S. suis to induce an inflammatory response in PMA-differentiated U937 macrophages, its effect on cell viability was evaluated. The MTT test revealed that macrophage viability was not significantly reduced (less than 20%) by a treatment with the recombinant SspA at a concentration of up to 33 μg/ml. As reported in Figure 1A-C, a significant dose-dependent secretion of all three pro-inflammatory cytokines IL-1β, IL-6 and TNF-α was observed following stimulation of macrophages with the recombinant SspA. More specifically, treatment of macrophages with SspA at 0.33 μg/ml resulted in a 2-fold, 55-fold and 7-fold increase of IL-1β, IL-6 and TNF-α levels, respectively.

All proteins that showed altered abundance in the mutant returned to near wild-type levels in the revertant. Three proteins were found

to be significantly upregulated in the mutant. They were identified as HtrA (2.5-fold), Cj0998 (2.1-fold), and FlaA (2.0-fold). HtrA is a serine protease with homologs found in most bacteria. this website In E. coli, HtrA is located on the periplasmic side of the inner membrane [79, 80], has protease activity [81], and has some chaperone activity at low temperatures [82]. It is possible that C. jejuni HtrA is upregulated in the mutant in a compensatory manner due to an increase in unfolded protein in the periplasm resulting from the loss of a major periplasmic PPIase. Brondsted et al. [83] found that a C. jejuni HtrA mutant showed no change in motility or autoagglutination, but did have a decreased ability to adhere to and invade INT407 cells and also exhibited altered cell morphology. Cj0998 is annotated as mTOR inhibitor ‘putative periplasmic protein’ and is restricted primarily to the epsilon proteobacteria, although the function of this protein is currently unknown. FlaA is the major subunit of the C. jejuni flagellum, and the upregulation of FlaA is consistent with the increase in motility and invasion of INT407 cells seen in the cj0596 mutant. Three proteins were shown to be significantly downregulated in the cj0596 mutant. They were identified as

EF-Ts (2.9-fold), SOD (2.6-fold), and EF-Tu (two spots; 2.0-fold, 1.9-fold). Among proteins whose expression was lower in the cj0596 mutant, EF-Ts and EF-Tu are involved in protein translation. They may be downregulated in the mutant due to an increase in unfolded protein in the periplasm and this in turn may result in the late stage growth defect due to a general decrease in protein synthesis. As C. jejuni lacks a sigma-E response [22], the signalling mechanism that would be

responsible is unknown. SOD plays a role in protecting C. jejuni against damage from oxidative stress and mutation of sod in C. coli was found to decrease the ability of the bacterium to colonize the intestines of 1-day-old chicks [84]. The decreased levels of SOD in the cj0596 mutant may therefore play a role in the colonization defects seen in mice. Conclusion Cj0596 is a highly conserved protein whose expression Mannose-binding protein-associated serine protease in C. jejuni is induced at human body temperature. Bacteria lacking Cj0596 were found to exhibit changes in several virulence-related phenotypes, including motility and host cell invasion, as well as alterations in protein expression and a defect in mouse colonization. Acknowledgements This study was supported by National Institutes of Health grants AI055715 and AI058284 to SAT. We thank Rhonda I. Hobb for sharing her expertise regarding mouse colonization experiments, and members of the Thompson Lab for helpful comments and discussions.

The decision to recommend elective sigmoid colectomy after recovery from acute diverticulitis should be made on a case-by-case

basis (Recommendation 1 C). The overall rate of recurrence appears to be approximately 10 to 30% within a decade after a first documented attack and that the majority of patients who have a single episode of diverticulitis will not have another [145]. In one report involving an average follow-up NVP-LDE225 of 9 years with 2551 patients whose initial episode of diverticulitis was treated successfully without surgery, only 13% had recurrent attacks and only 7% required colectomy [146]. These observations imply that routine elective colectomy is probably unwarranted if the disease is successfully managed on initial presentation and that surgical treatment should be limited to patients whose symptoms persist despite conservative therapy [147]. Thus, continued observation may be appropriate find more for most patients who have repeated attacks of uncomplicated diverticulitis. Systemic antibiotic treatment alone is usually the

most appropriate treatment for patients with a small (<4 cm in diameter) diverticular abscess and image guided percutaneous drainage is for those with a large (>4 cm in diameter) one (Recommendation 2 B). For patients in whom diverticulitis is complicated by peridiverticular abscess formation, the size of the abscess is an important determinant of the need for percutaneous drainage [145]. Many patients who have small pericolic abscesses

(4 cm or less in diameter) without peritonitis (Hinchey stage 1) can be treated conservatively with bowel rest and broad-spectrum antibiotics [148]. For patients with peridiverticular abscesses that are larger than 4 cm in diameter (Hinchey stage 2), observational studies indicate that CT-guided percutaneous drainage can be beneficial [149–160]. This procedure typically eliminates or reduces the size of the abscess [148, 151, 152], with a reduction in pain, resolution of leukocytosis, and defervescence usually seen within several days [153]. Percutaneous drainage may allow for elective rather than emergency surgery, increasing the likelihood of a successful one-stage procedure. Patients whose ZD1839 mouse abscess cavities contain gross feculent material tend to respond poorly, and early surgical intervention is usually required. Elective colon resection should typically be advised if an episode of complicated diverticulitis is treated non-operatively (Recommendation 2 C). After percutaneous drainage of a diverticular abscess, a later colectomy usually should be planned, because 41 percent of patients will otherwise develop severe recurrent sepsis [154]. Some, but not all, retrospective studies suggest that the number of recurrences is associated with the chance that emergency surgery will be required at some point in the future [155].

However, due to the heterogeneity of sample material derived from biogas reactors a control of cell counts with the Coulter Counter system before and after purification procedures was not feasible. Thus, a pure E. coli culture was used to control possible cell losses during the different procedures (Figure 1A). Figure 1 Influencing factors of purifications treatments on cell counts determined by Coulter Counter. (A)

Cell counts for E. coli cultures before (black bars) and after (gray bars) purification procedures. Denomination of procedures is according to Table 1. Error bars resulted from nine different measurements. (B) Influence of filtration: Cell counts of E. coli purified with procedure 1-C2-S2-H1-F2 prior to vacuum filtration with a 12–15 μm filter (black bar), after filtration (grey bar), and cell counts of residues on the filter (white bar). Error Selleck EPZ015666 bars resulted from three different measurements. Table 1 Purification procedures and modifications Procedures References Detergents Detergent concentrations (C) Ultrasound treatment (S)1) Homogenization (H)2) Filtration (F) 1 S.B. Singh-Verma (1968), LR. Bakken (1985) Sodium hexametaphosphate C1) 0,2% (w/v) S1) 40 W, 60 sec, 5 impulses/sec (different repetitions) H1) none F1 none     C2) 0,5% (w/v) S2) 65 W, 60 sec, 5 impulses/sec (different repetitions) H2) 60 sec, speed 5 (different repetitions) F2) 12–15

Pexidartinib purchase μm filter 2 S.B. Singh-Verma Dichloromethane dehalogenase (1968), LR. Bakken (1985) Bromhexine hydrochloride C1)

0,2% (w/v) S1) 40 W, 60 sec + 65 W, 60 sec, 5 impulses/sec H1) none n.a.         H2) 2× 60 sec, speed 5   3 W.B. Yoon and R.A. Rosson (1990) Tween C1) 5 μg/ml S1) 15 W, 30 sec, 5 impulses/sec H1) none n.a.     C2) 10 μg/ml S2) 35 W, 30 sec, 5 impulses/sec H2) 5 min, speed 5       C3) 25 μg/ml       4 E.L Schmidt (1974) Tween 80 + 0.007 g ml-1 flocculation reagent (Ca (OH)2: MgCO3 (2:5)) C1) 25 μl/ml n.a. n.a. n.a. 5 O. Resina-Pelfort et al. (2003) Triton X-100 C1) 10 μg/ml S1) 35 W, 30 sec, 5 impulses/sec H1) none n.a.     C2) 20 μg/ml S2) 45 W, 30 sec, 5 impulses/sec H2) 5 min, speed 5   6 L R. Bakken (1985) Sodium pyrophosphate C1) 0,2% (w/v) S1 3× 40 W, 60 sec, 5 impulses/sec H1) 3× 60 sec, speed 5 n.a. n.a. = not applied. 1)using the Sonoplus GW2070 (Bandelin, Germany). 2)using the dispersion unit VDI12 for 0.1 – 5.0 ml volumes (VWR, Germany). C1-3, H1-2, S1-2 and F1-2 indicate variations of the original protocols tested for their eligibility on samples from pure cultures and the UASS biogas reactor. With exception of procedure 4-C1 and 5-C2-S2-H1 (see Table 1 for details) the cell losses of control samples during purification were marginal. Best results were obtained with procedure 1, using sodium hexametaphosphate as detergent, and procedure 6, with sodium pyrophosphate as detergent (Figure 1A).

PubMed 7. Alshawi JS: Recurrent sigmoid volvulus in pregnancy: report of a case and review of the literature. Dis Colon Rectum 2005, 48:1811–1813.PubMedCrossRef 8. De U, De KK: Sigmoid volvulus complicating pregnancy. Indian J Med Ponatinib price Sci 2005, 59:317–319.PubMedCrossRef

9. Joshi MA, Balsarkar D, Avasare N, Pradhan C, Pereira G, Subramanyan P, et al.: Gangrenous sigmoid colon in a pregnant woman. Trop Gastroenterol 1999, 20:141–142.PubMed 10. Lurie S, Katz Z, Rabinerson D, Simon D: Sigmoid volvulus after medical management with subsequent operative laparoscopy of unruptured ectopic pregnancy. Gynecol Obstet Invest 1997, 43:204–205.PubMedCrossRef 11. Lord SA, Boswell WC, Hungerpiller JC: Sigmoid volvulus in pregnancy. Am Surg 1996, 62:380–382.PubMed 12. Allen JC: Sigmoid volvulus in pregnancy. J R Army Med Corps 1990, 136:55–56.PubMed 13. Keating JP, Jackson DS: Sigmoid volvulus in late pregnancy. J R Army Med Corps 1985, 131:72–74.PubMed 14. Hofmeyr GJ, Sonnendecker EW: Sigmoid volvulus in advanced pregnancy. Report of 2 cases. S Afr Med J 1985, 67:63–64.PubMed 15. Fraser JL, Eckert LA: Volvulus complicating pregnancy. Can Med Assoc J 1983, 128:1045–1048.PubMed 16. Fuller LDE225 mw JK, Larrieu AJ: Sigmoid volvulus in the young: a case following

cesarean section. Arch Surg 1978, 113:316–317.PubMedCrossRef 17. Lazaro EJ, Das PB, Abraham PV: Volvulus of the sigmoid colon complicating pregnancy. Obstet Gynecol 1969, 33:553–557.PubMed Exoribonuclease 18. Harer WB, Harer WB: Volvulus complicating pregnancy and puerperium; report of three cases and review of literature. Obstet Gynecol 1958, 12:399–406.PubMed 19. Kohen SG, Briele HA, Douglas LH: Volvulus in pregnancy. Am J Obst & Gynec 1944, 48:398. 20. Lambert AC: Paris thesis. 1931. 21. Ballantyne GH, Brandner MD, Beart RW, Ilstrup DM: Volvulus of the colon. Incidence and mortality. Ann Surg 1985, 202:83–92. 22. Kennedy A: Assessment of acute abdominal pain in the pregnant patient. Semin Ultrasound CT MR 2000, 21:64–77.PubMedCrossRef 23. Toppenberg KS, Hill DA, Miller DP: Safety of radiographic imaging

during pregnancy. Am Fam Physician 1999, 59:1813–1818.PubMed 24. Timins JK: Radiation during pregnancy. N J Med 2001, 98:29–33.PubMed 25. Karam PA: Determining and reporting fetal radiation exposure from diagnostic radiation. Health Phys 2000, 79:S85-S90.PubMedCrossRef 26. Chen MM, Coakley FV, Kaimal A, Laros RK: Guidelines for computed tomography and magnetic resonance imaging use during pregnancy and lactation. Obstet Gynecol 2008, 112:333–340.PubMedCrossRef 27. Allen JR, Helling TS, Langenfeld M: Intraabdominal surgery during pregnancy. Am J Surg 1989, 158:567–569.PubMedCrossRef 28. Redlich A, Rickes S, Costa SD, Wolff S: Small bowel obstruction in pregnancy. Arch Gynecol Obstet 2007, 275:381–383.PubMedCrossRef Competing interests The author declares that they have no competing interest. Authors’ contribution MRK conceived the study. SR collected the data and prepared the initial manuscript.