Authors’ contributions AJM-R and JJF conceived and designed the experiments.

AJM-R conducted the experiments. AG-O and AH-C conducted the AFM work and processed the results from AFM measurements. AM conducted the CLSM work. RD-G carried out the statistical analysis. VSM and MN contributed with reagents, materials and valuable advice in the experimental design. AJM-R, AG-O, AH-C and JJF analysed the data. AJM-R and JJF wrote APO866 datasheet the paper. All authors read and approved the final manuscript.”
“Background Methanogen diversity has been widely investigated across a range of ruminants by using clone library sequence approaches and many unknown methanogen 16S rRNA sequences have been uncovered. Tajima et al. [1] investigated the diversity of bovine rumen fluid using two different

selleck products archaea-specific primer sets, and for the first time reported the existence of a novel cluster of uncultured archaeal sequences which were distantly associated with Thermoplasma. However, the authors concluded that these novel sequences were likely from click here transient microbiota contaminating the animal feed, probably scavenging in an ecological niche in the rumen. Wright et al. [2] was the first to verify that these novel Thermoplasma-affiliated sequences were derived from the rumen when they investigated the diversity of rumen methanogens from sheep. The authors suggested a new order of methanogens for these novel sequences in the new cluster. The same authors [3] further found that over 80% of the total methanogen clones (63 of 78 clones) from the rumen of Merino sheep in Australia were 72–75% similar to Thermoplasmaacidophilum and Thermoplasmavolcanium. They [4] also found that about 50% of the total clones from methanogen 16S rRNA gene library Thalidomide of potato-fed feedlot cattle were present in the new cluster, and 38% for corn-fed feedlot cattle. Huang et al. [5] found that Thermoplasmatales-affiliated sequences dominated in the yak and cattle methanogen clone libraries, accounting for 80.9% and 62.9% of the sequences in the two libraries, respectively. Our previous study [6] on the

diversity of methanogens in the rumen of Jinnan cattle showed that Thermoplasmatales-affiliated sequences were widely distributed in the rumen epithelium, rumen solid and fluid fractions. In addition, ruminant-derived sequences in this new cluster were also found in other studies [4, 7–12]. Based on the analysis of the global data set, Janssenand Kirs [13] placed the majority (92.3%) of rumen archaea detected in total rumen contents into three genus-level groups: Methanobrevibacter (61.6%), Methanomicrobium(14.9%), and a large group of uncultured rumen archaea affiliated with Thermoplasmatales (15.8%), and named the uncultured archaea group in the rumen, for the first time, as Rumen Cluster C (RCC). Using RCC specific DGGE, clone library analysis and quantitative real-time PCR, Jeyanathan et al.

Publication bias was assessed by visual inspection of funnel plots [9], in which the standard error of log (OR) of each study was plotted against its log (OR). An asymmetric plot indicates a possible publication bias. The symmetry of the funnel plot was further evaluated by Egger’s linear regression test [10]. Statistical analysis was undertaken using the program STATA 11.0 software (Stata Corporation, Texas). Results Study characteristics

Relevant publications were SCH772984 nmr retrieved and screened originally. A total of seventy-eight publications were identified, of which sixty irrelevant papers were excluded. As shown in Figure1, eighteen publications were preliminary eligible, of which four publications not being case–control studies [11–14] and one article not presenting sufficient information [15] were discarded. Next, two studies [16, 17] whose genetic distributions of the control groups exhibited evident deviation from HWE were excluded. Then, one duplicate publication [18] which concerned the same research with one of the included click here studies [19] was further excluded. Lastly, ten case–control

studies were selected for data extraction [19–28]. Figure 1 The flow diagram of included/excluded studies. Of the selected publications, one was written in Chinese [24] while the remaining nine were in English. The relevant Dimethyl sulfoxide information was listed in Table1. According to this table, the first author and the number and BIRB 796 datasheet characteristics of cases and controls for each study as well as other necessary information are presented. Table 1 Characteristics of studies included in the meta-analysis First Author Publication Year Number of Leukemia Cases (male/female) Number of Controls (male/female) Number of AML cases Type of controls

Median (or mean) age, (range) year (Cases/Controls) Racial decent Country Balta 2003 33 (19/14) 185 (120/65) 33 AML Healthy controls (PB) 8.7(1–17)/7.4(0.58-17) Mixed Turkey D’Alo 2004 193 (107/86) 273(147/126) 193 AML Healthy controls (PB) 62(19–87)/60(19–90) Caucasian Italy Clavel 2005 219 (129/90) 105 (57/48) 28 AML Non-cancer controls (age,- gender-, hospital-, ethnicity-matched; HB) NA(0–15)/NA(0–15) Mixed France Aydin-Sayitoglu 2006 249 (143/106) 140 (73/67) 50 adult AML; 44 pediatric AML Healthy controls (PB) Adult:33(19–75); pediatric: 7.8(2–18)/28.7(16–59) Caucasian Turkey Bolufer 2007 443 (223/190) 454 (223/231) 302 AML Healthy controls (PB) 39.48(0.8-84)/38.

Fig. 1 The effect of N-ethyl-3-amino-5-oxo-4-phenyl-2,5-dihydro-1H-pyrazole-1-carbothioamide compound on biofilms formation by Haemophilus spp. on the basis of MBIC/MIC ratio Figure 2 shows the activity of N-ethyl-3-amino-5-oxo-4-phenyl-2,5-dihydro-1H-pyrazole-1-carbothioamide on the growth or biofilm formation by penicillinase-negative (S85Pen−) and penicillinase-positive (S86Pen+) H. parainfluenzae. In the case of penicillinase-positive isolate, the activity of the compound was significantly higher both on the growth and on the biofilm formation. Fig. 2 The effect of N-ethyl-3-amino-5-oxo-4-phenyl-2,5-dihydro-1H-pyrazole-1-carbothioamide compound

and ampicillin on the penicillinase-negative (filled diamond S85Pen−) and penicillinase-positive Stattic order (filled square S86Pen+) Haemophilus parainfluenzae planktonic or biofilm-forming cells (broth without bacteria: OD570 = 0.09–0.11) The in vitro cytotoxicity of the tested N-ethyl-3-amino-5-oxo-4-phenyl-2,5-dihydro-1H-pyrazole-1-carbothioamide compound was presented as percentage viability of vero cells used as an experimental model. According to the results shown in Table 2, after 48 h of incubation, no cytotoxic effect was observed up to 200 μg ml−1 concentration of the tested compound. The most widely used as a measurement of compound’s toxicity is the half maximal effective concentration (EC50), as the concentration of the selleck kinase inhibitor compound where

Y27632 50 % of its maximal effect is observed; in case of the tested compound EC50 = 278.8 μg ml−1. This means that this compound was not toxic to eukaryotic cells at concentrations exerting inhibitory effect against Haemophilus spp., including anti-biofilm activity. Table 2 The effect of N-ethyl-3-amino-5-oxo-4-phenyl-2,5-dihydro-1H-pyrazole-1-carbothioamide on vero cells line viability Compound concentration (μg ml−1)

Cell viability (in %) ± SD x 500 37.95 ± 7.7 200 82.15 ± 5.7 100 89 ± 6.6 50 93.55 ± 4.2 25 97.4 ± 1.7 12.5 98.05 ± 1.8 6.25 98.75 ± 2.0 3.15 100 ± 0.0 0 (control) 100 ± 0.0 Although the control of bacterial infections has been effective since the discovery of antimicrobial drugs, widespread drug resistance among bacteria has led to a search for new ZD1839 clinical trial antibacterial agents. However, the finding of biofilm phenotype bacteria, showing usually intrinsic insensitivity to available drugs at standard dosing effective against planktonic cells, has created a necessity to pay more attention to targeted anti-biofilm agents. In this work, we have found that the N-ethyl-3-amino-5-oxo-4-phenyl-2,5-dihydro-1H-pyrazole-1-carbothioamide possessed good in vitro activity either against free-floating (planktonic) or biofilm-forming cells of Haemophilus spp. Haemophili rods, e.g., pathogenic H. influenzae or opportunistic H. parainfluenzae are found to be a part of proper microflora of the upper respiratory tract (Kilian, 2007; Murphy et al., 2007).

(C) Spectrum of pure methyl parathion (control experiment). The newly found peak might be due to the 4-nitrophenolate ions which are produced by the hydrolysis of methyl parathion in alkaline medium [20]. It is known that due to the catalytic hydrolysis of methyl parathion, two hydrolyzed products, 4-nitrophenolate ions and sodium di-O-methyl thiophosphonate are produced (Figure 1). The literature confirms that 4-nitrophenolate ion shows a characteristic absorption peak at 400 nm [21]. The increase in the concentration of methyl parathion in the mixture quantitatively increases the amount of the 4-nitrophenolate ions in the medium which are reflected in the absorption spectra (Figure 3A). A calibration curve between

the absorption

coefficient of the 400-nm peak and the concentration of the pesticide allows quantitative estimation of the methyl parathion SIS3 clinical trial present in a sample at ppm levels (Figure 3B). This calibration curve enables the estimation of methyl parathion indirectly by estimating the 4-nitrophenolate ions present in the medium. The corresponding decrease in the absorption peak of GNP at 532 nm may be due to the agglomeration of GNP which is selleck kinase inhibitor facilitated by the presence of the other hydrolyzed product sodium di-O-methyl thiophosphonate containing sulfur. The formation of agglomeration of GNP is indicated by the broadening of the 532-nm peak in the presence of methyl parathion. A control experiment (Figure 3C) was carried out by CBL-0137 mouse taking methyl parathion only, and no peak was Pyruvate dehydrogenase lipoamide kinase isozyme 1 found at 400 nm. The peak at 400 nm emerges only when the hydrolysis of methyl parathion occurs in the presence

of GNP in water. Figure 4A shows the TEM images of GNP produced from a 5:5 composition of tomato extract. The particles are mostly spherical, and their sizes varied from 5 to 20 nm. A histogram plot (Figure 4B) shows the distribution of particles of different sizes. Selected area diffraction (SAED) pattern shown in Figure 4C illustrates the crystalline nature of GNP. Figure 4 TEM micrographs, particle size distribution histogram, and SAED pattern of GNP. (A) TEM micrographs of GNP with tomato extract. (B) Particle size distribution histogram of spherical GNP, and (C) corresponding SAED pattern of GNP. Figure 5A shows the representative TEM images of GNP with SDS in alkaline medium. The histogram of it is shown in Figure 5B. The significant changes are observed in the size of the particles. The particles become of uniform sizes, and the sizes reduced to 5 to 10 nm. SDS, being a strong capping agent stabilizes the gold nanoparticles as soon as nucleation happens and thereby restricts the nanoparticles to a finite size. As a result, nearly monodispersed gold nanoparticles of sizes 5 to 10 nm were obtained. Figure 5 TEM micrographs, particle size distribution histogram, SDS-capped GNP with methyl parathion, and SAED pattern of GNP. (A) TEM micrographs of SDS-capped GNP with tomato extract.

Acknowledgements We thank Chung CD for excellent technical support and helpful discussions of the data. This work was funded by grant from National Science Council of Taiwan. References

1. Sorensen GV, Erichsen R, Svaerke C, Farkas DK, Sorensen HT: Risk of cancer in patients with inflammatory bowel disease and venous thromboembolism: a nationwide cohort study. Inflammatory bowel diseases 2012,18(10):1859–1863.PubMedCrossRef Belinostat clinical trial 2. Baumgart DC, Carding SR: Inflammatory bowel disease: cause and immunobiology. Lancet 2007,369(9573):1627–1640.PubMedCrossRef 3. Parkes GC, Sanderson JD, Whelan K: Treating irritable bowel syndrome with probiotics: the evidence. Proc Nutr Soc 2010,69(2):187–194.PubMedCrossRef 4. McFarland LV, Dublin S: Meta-analysis of probiotics Semaxanib cell line for the treatment of irritable

bowel syndrome. World J Gastroenterol 2008,14(17):2650–2661.PubMedCrossRef 5. Arseneau KO, Tamagawa H, Pizarro TT, Cominelli F: Innate and adaptive immune responses related to IBD pathogenesis. Curr Gastroenterol Rep 2007,9(6):508–512.PubMedCrossRef 6. Peng S, Lin JY, Lin MY: Antiallergic effect of milk fermented with lactic acid bacteria in a murine animal model. J Agric Food Chem 2007,55(13):5092–5096.PubMedCrossRef 7. Li CY, Lin HC, Lai CH, Lu JJ, Wu SF, Fang SH: selleck products immunomodulatory effects of Lactobacillus and Bifidobacterium on both murine and human mitogen-activated T cells. Int Arch Allergy Immunol 2011,156(2):128–136.PubMedCrossRef 8. Ou CC, Lu TM, Tsai JJ, Yen JH, Chen HW, Lin MY: Antioxidative effect of lactic acid bacteria: intact cells vs. intracellular extracts. J Food Drug Anal 2009,17(3):209–216. 9. Loguercio C, Federico A, Tuccillo C, Terracciano F, D’Auria MV, De Simone C, Del Vecchio BC: Beneficial effects of a probiotic VSL#3 on parameters of liver dysfunction in chronic liver diseases. Edoxaban J Clin Gastroenterol 2005,39(6):540–543.PubMedCrossRef 10. Trebichavsky I, Rada V, Splichalova A, Splichal I: Cross-talk of human gut with bifidobacteria. Nutr Rev 2009,67(2):77–82.PubMedCrossRef 11. Golowczyc MA, Mobili P, Garrote GL, Abraham AG, De Antoni GL: Protective action of Lactobacillus kefir carrying

S-layer protein against Salmonella enterica serovar Enteritidis. Int J Food Microbiol 2007,118(3):264–273.PubMedCrossRef 12. Ou CC, Lin SL, Tsai JJ, Lin MY: Heat-killed lactic acid bacteria enhance immunomodulatory potential by skewing the immune response toward Th1 polarization. J Food Sci 2011,76(5):M260-M267.PubMedCrossRef 13. Chuang L, Wu KG, Pai C, Hsieh PS, Tsai JJ, Yen JH, Lin MY: Heat-killed cells of lactobacilli skew the immune response toward T helper 1 polarization in mouse splenocytes and dendritic cell-treated T cells. J Agric Food Chem 2007,55(26):11080–11086.PubMedCrossRef 14. Tandon P, Moncrief K, Madsen K, Arrieta MC, Owen RJ, Bain VG, Wong WW, Ma MM: Effects of probiotic therapy on portal pressure in patients with cirrhosis: a pilot study. Liver Int 2009,29(7):1110–1115.

Proc Natl Acad SciUSA 84:8414–8418 Schatz GH, Brock H, Holzwarth AR (1988) A kinetic and energetic model for the primary processes in photosystem II. Biophys J 54:397–405PubMed Schilstra MJ, Nield J, Dorner W, Hankamer B, Carradus M, Barter LMC, Barber J, Klug DR (1999) Similarity selleckchem between PRIMA-1MET nmr electron donor side reactions in the solubilized photosystem II-LHC II supercomplex and photosystem-II-containing membranes. Photosynth Res

60(2–3):191–198 Shimoni E, Rav-Hon O, Ohad I, Brumfeld V, Reich Z (2005) Three-dimensional organization of higher-plant chloroplast thylakoid membranes revealed by electron tomography. Plant Cell 17(9):2580–2586PubMed Standfuss R, van Scheltinga ACT, Lamborghini M, Kuhlbrandt W (2005) Mechanisms of photoprotection and nonphotochemical quenching in

pea light-harvesting complex at 2.5A resolution. EMBO J 24(5):919–928PubMed Tian L, van Stokkum IH, Koehorst RB, Jongerius A, Kirilovsky D, van Amerongen H (2011) Site, rate, and mechanism of photoprotective quenching in cyanobacteria. J Am Chem Soc 133(45):18304–18311. doi:10.​1021/​ja206414m PubMed Tian L, van Stokkum IH, Koehorst RB, van Amerongen H (2012) Light harvesting and blue-green light induced non-photochemical quenching in two different C-phycocyanin mutants of synechocystis PCC 6803. J Phys Chem. doi:10.​1021/​jp309570u Tian L, Farooq S, van Amerongen H (2013) Probing the picosecond https://www.selleckchem.com/products/EX-527.html kinetics of the photosystem II core complex in vivo. Phys Chem Chem Phys. doi:10.​1039/​c3cp43813a Umena Y, Kawakami K, Shen JR, Kamiya N (2011) Crystal structure of oxygen-evolving photosystem II at a resolution of 1.9 A. Nature 473(7345):55–60. out doi:10.​1038/​nature09913 PubMed Van Amerongen H, van Grondelle R (2001) Understanding the energy transfer function of LHCII, the major light-harvesting complex of green plants. J Phys Chem B 105(3):604–617 Van Amerongen H,

Kwa SLS, van Bolhuis BM, van Grondelle R (1994) Polarized fluorescence and absorption of macroscopically aligned light harvesting complex II. Biophys J 67:837–847PubMed Van Amerongen H, Valkunas L, van Grondelle R (2000) Photosynthenic excitons. World Scientific Publishing Co. Pte. Ltd, Singapore Van Amerongen H, Dekker JP, Parson WW, Green BR (2003) Light-harvesting antennas in photosynthesis. Kluwer Academic, The Netherlands, pp 219–251 van der Vos R, Carbonera D, Hoff AJ (1991) Microwave and optical spectroscopy of carotenoid triplets in light-harvesting complex LHCII of spinach by absorbance-detected magnetic resonance. J Appl Magn Reson 2:179–202 van der Weij-de Wit CD, Dekker JP, van Grondelle R, van Stokkum IH (2011) Charge separation is virtually irreversible in photosystem II core complexes with oxidized primary quinone acceptor. J Phys Chem A 115(16):3947–3956. doi:10.​1021/​jp1083746 PubMed van Grondelle R (1985) Excitation energy transfer, trapping and annihilation in photosynthetic systems.

“
“Background Wolbachia and Cardinium are intracellular bacteria infecting a wide range of arthropod species. They have been classified as reproductive parasites, being able to manipulate their host’s reproductive system in order to Lazertinib purchase promote their own transmission [1–3]. Recently, beneficial effects NCT-501 clinical trial of Wolbachia have been identified as well, as Wolbachia can protect hosts against virus infection [4, 5]. Cardinium may also exert beneficial effects [6] and in many other cases the effect of Wolbachia or Cardinium is unknown. Wolbachia is well

studied and is widespread among arthropods and nematodes. It is estimated that around 66% of all insects are infected with Wolbachia Proteases inhibitor [7]. This diverse genus has been subdivided into 11 “supergroups” (A-K)

on the basis of molecular phylogenetic analysis [8–13]. Cardinium was more recently discovered and has so far been found in 6-7% of all arthropods, though seems to be more common in Chelicerates than in insects [2, 14–18]. Wolbachia and Cardinium have been found co-infecting the same host species [2, 15, 17–21]. Although Wolbachia and Cardinium are generally considered to be clonally inherited via vertical transmission, there

is now a large body of molecular evidence for discordant phylogenies of host and endosymbiont [22–29]. Distantly related Wolbachia or Cardinium before strains can infect closely related host species, and closely related strains may infect distantly related host species. Such patterns suggest horizontal transmission of bacteria (or at least of some bacterial genes) between hosts, although direct evidence for horizontal transmission is rare [30–32]. Horizontal transfer has been further supported by evidence for recombination [33]. For Wolbachia, recombination has been found between genes (intergenic) as well as within genes (intragenic). Intergenic recombination is evident from inconsistencies between gene trees [34–36]. Intragenic recombination has been observed within the genes wsp, ftsZ, and gltA and within and between supergroups A and B [34, 37–41]. Recently, a genomic comparison of A-group Wolbachia strains by Klasson et al. [42] showed highly recombining genomes, implying frequent horizontal gene transfer.

N: nuclear fraction, C: cytosolic fraction, IB: immunoblot. LMP1 activated the activity of cyclin D1 promoter by the EGFR and STAT3 pathways Because cyclin D1 contains both EGFR and STAT3 binding sites adjacent within three nucleotides [31], we addressed whether nuclear accumulation and the interaction between EGFR and STAT3 check details at the cyclin D1 promoter was under the regulation of the oncoprotein LMP1. The effect of LMP1 on the transcriptional activation of cyclin D1 was examined using a luciferase reporter construct, pCCD1-wt-Luc, driven by the cyclin D1 promoter that contained

both EGFR and STAT3 binding sites (Figure  3A). First, we constructed a mutant cyclin D1 promoter luciferase reporter plasmid, pCCD1-mt-Luc, to which no transcription factors would bind at a cyclin D1 promoter region according to a database search (TFSEARCH, http://​www.​cbrc.​jp/​research/​db/​TFSEARCH) (Figure  3A). Then, we transfected the plasmid into CNE1 and CNE1-LMP1 cells, and LMP1 increased the cyclin D1 promoter activity while the mutant cyclin D1 promoter decreased the cyclin D1 promoter activity Mizoribine cost (column 5 and column 6 of Figure  3B). As shown in Figure  3B, EGFR increased the luciferase expression in CNE1-LMP1 cells (column 7) but not in CNE1 cells (column 3). Mutations in the cyclin D1 promoter

greatly (column 6) were attenuated its transcriptional activity Edoxaban in the presence of LMP1 while EGFR rescued the cyclin D1 promoter activity partially (column 8), indicating that LMP1 positively regulates the activity of the

cyclin D1 promoter under EGFR. Furthermore, data in Figure  3C demonstrate that STAT3 increased the activity of the cyclin D1 promoter in the presence of LMP1 (column 7 of Figure  3C) while the cyclin D1 promoter activity were decreased greatly after mutating the EGFR and STAT3 binding sites in the Cyclin D1 promoter (column 8 of Figure  3C), further indicating that LMP1 upregulates the activity of the cyclin D1 promoter through STAT3. Figure 3 Identification of an EGFR and STAT3 response element in the cyclin D1 promoter. (A) Schematic diagram of mutant cyclin D1 promoter constructs are shown. The SIS3 cell line expansion for EGFR and STAT3 binding site illustrates the wild-type sequence and frames the nucleotides replaced by mutations. (B-C) Dual luciferase-reporter assays were performed in LMP1-negative and LMP-positive CNE1 cells after co-transfection of a wild type or mutant cyclin D1 promoter-reporter construct, plasmids expressing wild-type EGFR or STAT3, and a Renilla luciferase transfection control plasmid. The fold induction by EGFR and STAT3 is displayed as the ratio of promoter activity obtained with wild-type compared to the DNA-binding mutant. (mean ± SD, n = 3, *p < 0.05, **p < 0.01). mt: mutation, wt: wild-type.

Regarding simple pre-post assessments of QoL in single-arm studies, it is probably unnecessary to state that

they are generally not appropriate for judging influences on QoL, since it is affected by many factors. Concerning survival (Table 3), some of the RCTs show a statistically significant benefit while others compound screening assay show a statistical trend or no difference. Most of the non-RCTs (which included larger patient numbers) show a major impact. The CA3 validity of the studies is limited because of their small sample size (median only 52 participants per RCT), and because 8 of the 9 RCTs were imbedded in the same (large) epidemiological cohort study. This study was started in the 1970s, before modern standards of data quality control (ICH-GCP, GEP) were established, and it therefore does not fulfil modern standards in this respect. The 9th RCT had enrolled more patients but was conducted even earlier, and suffers from a major attrition rate due to protocol violation [62]; the subsequent analysis followed the “”as treated”" instead of the “”intention-to-treat”" principle [145]. Hence Selleck CX 5461 bias cannot be excluded. None of the survival studies was blinded, but survival is generally not easily affected by observer bias or suggestive effects [138–140]. Seen altogether, although results were consistent, questions regarding survival

remain and validity of evidence is moderate at best. An independent, GCP-conform trial with sufficient power would be desirable to further evaluate potential survival benefit. Regarding tumour behaviour, evidence from RCTs is scanty; most benefits were shown in non-randomized studies. In single-arm studies of patients with no concomitant conventional cancer treatment, high-dose or local application of whole VAE led to substantial remission of tumour or malignant effusion. This was also observed in animal studies: local application resulted in tumour-growth inhibition and increased survival. However, this application and dosage is not standard and cannot be recommended widely

due to potential risks of high dose or local application. With ordinary Ribonucleotide reductase VAE application, schedule and dosage, spectacular tumour remissions tend to be the exception [20, 36]. No tumour remission was observed after application of rMLs. Remission in CIN cannot be distinguished from spontaneous remission rates, which are frequent in this indication. Apart from the discussed issues, the following validity aspects have to be considered: An attrition rate above 10% was present in 10 RCTs. In 5 of these RCTs [49–51, 53], patients were excluded before baseline assessment. Here the patients were provisionally enrolled into the matching and pairwise randomization procedure; subsequently they were asked for informed consent, and were excluded from the study if they declined, together with their matched twin.

PubMed 11. Gerstenecker B, Jacobs E: Topological mapping of the P1-adhesin of Mycoplasma Selleck MDV3100 pneumoniae with adherence-inhibiting monoclonal antibodies. J Gen Microbiol 1990,136(3):471–476.PubMedCrossRef 12. Razin S, Jacobs E: Mycoplasma adhesion. J Gen Microbiol 1992,138(3):407–422.PubMedCrossRef 13. Su CJ, Tryon VV, Baseman JB: Cloning and sequence analysis of cytadhesin P1 gene from Mycoplasma pneumoniae . Infect Immun 1987,55(12):3023–3029.PubMedCentralPubMed https://www.selleckchem.com/products/pp2.html 14. Svenstrup HF, Nielsen PK, Drasbek M, Birkelund S, Christiansen

G: Adhesion and inhibition assay of Mycoplasma genitalium and M. pneumoniae by immunofluorescence microscopy. J Med Microbiol 2002,51(5):361–373.PubMed 15. Chaudhry R, Varshney AK, Malhotra P: Adhesion proteins of Mycoplasma pneumoniae . Front Biosci 2007, 12:690–699.PubMedCrossRef 16. Krivan HC, Olson LD, Barile MF, Ginsburg V, Roberts DD: Adhesion of Mycoplasma pneumoniae to sulfated glycolipids and inhibition by dextran sulfate. J Biol Chem 1989,264(16):9283–9288.PubMed 17. Krause DC, Leith DK, Wilson RM, Baseman JB: Identification of Mycoplasma pneumoniae proteins associated with hemadsorption and virulence. Infect Immun 1982,35(3):809–817.PubMedCentralPubMed 18. Krause DC: Mycoplasma pneumoniae cytadherence: unravelling

the tie that binds. Mol Microbiol 1996,20(2):247–253.PubMedCrossRef 19. Seto S, Kenri T, Tomiyama T, Miyata M: Involvement of P1 adhesin in gliding motility of Mycoplasma IACS-10759 molecular weight pneumoniae as revealed by the inhibitory effects of antibody under optimized gliding conditions. J Bacteriol 2005,187(5):1875–1877.PubMedCentralPubMedCrossRef 20. Tabassum I, Chaudhry R, Chourasia BK, Malhotra P: Identification of N-terminal 27 kDa fragment of Mycoplasma pneumoniae P116 protein as specific immunogen in M. pneumoniae infections. BMC Infect Dis 2010,

10:350.PubMedCentralPubMedCrossRef 21. Chaudhry R, Nisar N, Hora B, Chirasani SR, Malhotra P: Vasopressin Receptor Expression and immunological characterization of the carboxy-terminal region of the P1 adhesin protein of Mycoplasma pneumoniae . J Clin Microbiol 2005,43(1):321–325.PubMedCentralPubMedCrossRef 22. Jacobs E, Fuchte K, Bredt W: Isolation of the adherence protein of Mycoplasma pneumoniae by fractionated solubilization and size exclusion chromatography. Biol Chem Hoppe Seyler 1988,369(12):1295–1299.PubMedCrossRef 23. Dallo SF, Su CJ, Horton JR, Baseman JB: Identification of P1 gene domain containing epitope(s) mediating Mycoplasma pneumoniae cytoadherence. J Exp Med 1988,167(2):718–723.PubMedCrossRef 24. Opitz O, Jacobs E: Adherence epitopes of Mycoplasma genitalium adhesin. J Gen Microbiol 1992,138(9):1785–1790.PubMedCrossRef 25. Jacobs E, Pilatschek A, Gerstenecker B, Oberle K, Bredt W: Immunodominant epitopes of the adhesin of Mycoplasma pneumoniae . J Clin Microbiol 1990,28(6):1194–1197.PubMedCentralPubMed 26.