, HS1165: 36. Benson G: Tandem repeats finder: a program to analyze DNA sequences. Nucl Acids Res 1999,27(2):573–58.PubMedCrossRef 37. Peakall R, Smouse P: GENALEX 6: Genetic analysis in Excel. Population genetic software for teaching and research. Mol Ecol Notes 2006, 6:288–295.CrossRef

38. Raymond M, Rousset F: GENEPOP (version 1.2): population genetics software for exact tests and ecumenicism. J Hered 1995, 86:248–249. 39. Tamura K, Dudley J, Nei M, Kumar S: MEGA4: Molecular evolutionary genetics analysis (MEGA) software Version 4.0. Mol Biol Evol 2007,24(8):1596–1599.PubMedCrossRef 40. Pritchard J, Stephens M, Donnelly P: Inference of population structure using multilocus genotype data. Genetics 2000, 155:945–959.PubMed 41. Jakobsson M, Rosenberg NA: CLUMPP: a cluster matching and CFTR activator permutation program for dealing with label switching and multimodality in analysis of population Eltanexor structure. Bioinformatics 2007, 23:1801–1806.PubMedCrossRef 42. Rosenberg NA: DISTRUCT: a program for the graphical display of population structure. Mol Ecol Notes (2004) 2004, 4:137–138.CrossRef Authors’ contributions HL, MSI, JMG, YPD, HDC, GK and ELC coordinated the study, collected selleck kinase inhibitor samples

and provided preliminary data. HL, JMG, and YB carried out genotyping of HLB samples. MSI, JMG and HL analyzed results and wrote the paper. All authors read and approved the final manuscript.”
“Background The zebrafish (Danio rerio) is a small tropical teleost that bridges the phylogenetic evolutionary Astemizole gap between invertebrates and mammals

in experimental biomedicine. It is evolutionarily closer to humans than fruit flies and nematodes, and is easier to work with and study than mice [1]. Recently, increased interest in using zebrafish for studies of human diseases as disparate as cancer, microbial infections and immune-pathological changes has evolved [2]. As an infection model, zebrafish have been employed for study of both human and fish pathogens [1, 3–6]. Aeromonas hydrophila is a ubiquitous Gram-negative aquatic bacterium and opportunistic pathogen causing fatal hemorrhagic septicemia in several fish species including warm water and temperate aquaculture species [7–9]. In particular, A. hydrophila infections have been repeatedly reported from zebrafish facilities causing unusual [10] and sometimes high mortality rates [11]. Some strains of A. hydrophila have also been reported to be important human pathogens [12]. Conjugative R plasmids assigned to the IncU incompatibility group are widespread in environmental and fish pathogenic Aeromonas species worldwide [13]. An IncU representative, pRAS1, was detected in Aeromonas salmonicida from Norway [14]. This plasmid is very similar to an IncU plasmid derived from a human urinary tract pathogenic Escherichia coli in Eastern Germany as early as the 1970′s [15].

The product ion at m/z 469 is most probably derived PFT�� from m/z 402 fragment ion of SPhMDPOBn: [M-C10H11O2-C6H5S + 3Na+-2H+]+. The ion at m/z 247 was identified as [M + 3Na]3+/3. Figure 2 The positive-mode ESI IT mass spectrum of О -(phenyl-2-acetamido-2,3-dideoxy-1-thio-β- d -glucopyranoside-3-yl)- d -lactoyl-

l -alanyl- d -isoglutamine (SPhMDPOBn). TPD-MS analysis of О-(phenyl-2-acetamido-2,3-dideoxy-1-thio-β-d-glucopyranoside-3-yl)-d-lactoyl-l-alanyl-d-isoglutamine As can be seen from the P-T curve (Figure 3), pyrolytic degradation of thiophenylglycoside of MDP in the pristine state proceeds in a relatively narrow temperature range from 150°С to 250°С in two main stages (Figure 4). The same two main stages are observed on the TPD-curves (Figure 5). Probably, these stages of pyrolysis result from the existence of SPhMDPOBn in α- and β-anomeric forms. Figure 4 Selleckchem Ricolinostat illustrates a possible pyrolytic pattern and products. Figure 3 Galunisertib mouse Temperature-pressure ( P – T ) curve of SPhMDPOBn in the pristine state. P, pressure of the volatile products; T, temperature of SPhMDPOBn. Figure 4 Pyrolysis pattern of SPhMDPOBn under TPD-MS conditions in the pristine state. Figure 5 Pyrolysis of

SPhMDPOBn in the pristine state. (A) Mass spectrum of the pyrolysis products at 163°C, obtained after electron impact ionization. (B) Mass spectrum of the pyrolysis products at 194°C, obtained after electron impact ionization. (C) Thermograms for m/z 124, 110, 108, 91, 84, 79, 77, and 66 under pyrolysis of О-(phenyl-2-acetamido-2,3-dideoxy-1-thio-β-d-glucopyranoside-3-yl)-d-lactoyl-l-alanyl-d-isoglutamine (SPhMDPOBn) in the pristine state. At the first and the second stages (Figure 5), the elimination of the benzyl ester-protected carboxylic group of isoglutamine fragment takes place, which gives rise to a peak of the molecular ion of benzyl alcohol at m/z 108 (Figure 4). Fragmentation of benzyl alcohol via loss of the -OH group at m/z 17 leads to a common fragment

seen for alkyl benzenes at m/z 91. Loss of CH2OH at m/z 31 from the molecular ion gives m/z 77 corresponding to the phenyl cation (Figure 4). Loss of aglycone and carbohydrate moiety occurs during the first and the second stages Adenosine of pyrolysis. But it is observed that there are different ratios of peak intensities on the TPD-curve for molecular and fragment ions of corresponding products. Thus, the first stage proceeds via preferential removal of benzyl alcohol, while the second stage-by elimination of thiophenol. Aglycon is easily removed in the form of thiophenol under the pyrolysis of SPhMDPOBn. The intensity of a thiophenol molecular ion peak is high as the thiophenol molecular ion is stable. The thiophenol molecular ion is stabilized by the presence of π-electron systems, which are capable of accommodating a loss of one electron more easily. The fragmentation of thiophenol molecular ion under electron impact is shown in Figure 6.

J Microbiol Methods 2009, 78:265–270.PubMedCrossRef 68. Dietrich R, Moravek M, Burk C, Granum PE, Märtlbauer E: Production and characterization of antibodies against each of the three subunits of the Bacillus cereus nonhemolytic enterotoxin complex. Appl Environ Microbiol 2005, 71:8214–8220.PubMedCrossRef Authors’ contributions AF participated in the study design, constructed plasmids and mutants,

performed cytotoxicity assays, and wrote the manuscript. AF and TL performed transformations, sampling and Western blot analysis, and TL participated in writing of the manuscript. PEG conceived buy H 89 of the study, participated in its design, and critically revised the manuscript. All authors read and approved the final manuscript.”
“Background selleck chemical Vibrio cholerae is the etiological agent of the severe diarrheal disease cholera. Similar to many Gram-negative enteric pathogens, horizontal gene transfer and recombination plays a

significant role in the evolution and emergence of new pathogenic strain of this species [1–12]. The main cause of the explosive rice water diarrhea characteristic of cholera is the cholera toxin (CT), an AB type enterotoxin, which is encoded within the ssDNA filamentous phage CTXɸ [13, 14]. The B subunit of CT binds to the GM1 gangliosides, which are exposed when higher order gangliosides found in the intestinal mucus are cleaved by sialidase/neuraminidase (NanH). This protein is encoded NU7441 molecular weight within a 57 kb region named Vibrio Pathogenicity Island-2 (VPI-2) [15, 16]. In addition to encoding sialidase, VPI-2 also encodes the sialic acid catabolism (SAC) gene cluster (Figure 1A) [16–19]. The SAC cluster

was shown find more to be present only in pathogenic isolates of V. cholerae and enables the bacterium to grow on sialic acid as a sole carbon source [18, 20]. Recently, we demonstrated that the ability to catabolize sialic acid gives V. cholerae a competitive advantage in vivo [19]. In non-O1/O139 pathogenic isolates, in addition to the SAC cluster are the genes required for a type 3 secretion system which is important for virulence [21–25]. The toxin co-regulated pilus (TCP), an essential intestinal colonization factor for V. cholerae, is encoded within the 40 kb Vibrio Pathogenicity Island-1 (VPI-1 or TCP Island) region [26, 27]. Figure 1 Vibrio Pathogenicity Island-2 (VPI-2) ORFs and primers used in this study. A. Schematic representation of VPI-2. Small black vertical arrows mark ORFs VC1758 (IntV2), VC1785 (VefA), or VC1809 (VefB). Block arrows represent ORFs and direction of transcription. Black arrows represent core genome ORFs (VC1757 and VC1810) present in all V.

Φ2954 has the sequence of GC at the 5′ termini of segments S and M and ACAA at the 5′ terminus of L. Bacteriophage Φ8 and its close relatives have identical sequences, click here GAAAUUU, at the 5′ termini of all three transcripts [8]. The 3′ sequences of the three plus strands contained a 55 base near identity at the terminus. This sequence produced a structure with two hairpin stem loops that differ in sequence from those of phi12 and other members of the Cystoviridae but probably function as protection against host exonucleases (Fig. 4) [9]. Amino acid similarity to some of the proteins of the Φ6 L segment was also found, but at a lower level than found for Φ12 (Table 1).

An exception was the finding that protein P10 had striking similarity to P10 of Φ13, a phage that otherwise had little similarity to Φ2954 (Table 1). A strong relationship was found between the product of Selleck Thiazovivin this website gene 5 and protein FlgJ (GI:71555478) of the host organism P. syringae. Protein P5 is a muramidase in all the Cystoviridae while FlgJ is a host flagellar protein that has peptidoglycan hydrolase activity. The similarity of Φ2954 P5 to FlgJ is greater than that of Φ2954 to that of P5 protein of any of the other cystoviruses, even Φ12. It seems clear that gene5 was derived from the host muramidase gene. The Cystoviridae are capable of acquisition of genetic material from the host. Although

acquisition Urocanase is much more likely if pac sequences are on the introduced RNA, we have shown acquisition in cases where pac sequences are not present [10]. Figure 1 Bacteriophage Φ2954 was purified by zone and equilibrium centrifugation in sucrose gradients and applied to an 18% polyacrylamide gel for electrophoresis. The gel was stained with Coomasi blue. Purified Φ6 virions were displayed for comparison. Figure 2 Genetic maps of the genomic segments of Φ2954. Restriction sites utilized in the construction of phage variants are shown. PstI and XbaI sites are present in the plasmid vectors for the cDNA copies. Figure 3 Sequence comparisons at the 5′ termini of transcripts of Φ2954,

Φ12 and Φ6. Note that in each case the sequence of L is different from those of S and M. Figure 4 Stem loop structures at the 3′ termini of the Φ2954 transcripts. Table 1 Comparison of amino acid sequences of Φ2954 proteins to those of Φ12, Φ6, Φ13 and FlgFa Protein Similarity to Φ12 Identity to Φ12 Similarity to Φ6 Identity to Φ6 Similarity to FlgFb P1 60 40 nss     P2 66 50 38 24   P3 nssc   nss     P4 63 45 41 25   P5 47 25 38 24 54/36 P6 nss   nss     P7 55 33 nss     P8 45 29 nss     P9 51 33 nss     P10 nss   nss 71d 57d   P16 nss nss nss     P12 57 30 nss     P14 nss   nss     P15 nss         a Needleman-Wunsch alignment b P. syringae FlgJ glycosidase [GenBank AAZ34689.1] c no significant similarity d relationship to Φ13 The arrangement of the genes is similar to that of most of the Cystoviridae [11].

Apoptosis assay Apoptosis was evaluated using Annexin V-FITC/PI apoptosis detection kit purchased from BIO-BOX Biotech (Nanjing, China) following the manufacturer’s instructions. Briefly, 2×106cells were harvested and washed twice with pre-cold PBS and then resuspended in 500 μl binding buffer. 5 μl of annexin V-FITC and 5 μl of Propidium Iodide (PI) were added to each sample and then incubated at room temperature in dark for 10 minutes. Analysis was performed by FACScan flow cytometer (Becton Dickinson, San Jose, CA). Results Parthenolide effectively inhibits the growth of human lung cancer cells through Dibutyryl-cAMP induction of apoptosis and cell cycle arrest It has

been reported that parthenolide has antitumor effects on various cancer cells. Hence, we examined the inhibition effect of PTL on Akt inhibitor human NSCLC cells by treating the cells with various concentrations for 48 h and then

conducting SRB and MTT assay. As is shown, PTL had a dose-dependent growth inhibition effect on NSCLC cells Calu-1, H1792, A549, H1299, H157, and H460 (Figure 1A, B). To characterize the mechanism by which PTL induces growth inhibition in human NSCLC cells, we first determined the effect of PTL on induction of Caspase Inhibitor VI apoptosis by western blot analysis. The data showed that PTL could induce cleavage of apoptotic proteins such as CASP8, CASP9, CASP3 and PARP1 both in concentration- and time-dependent manner in tested lung cancer cells, indicating that apoptosis was trigged after PTL exposure (Figure 1C, D). In addition to induction of apoptosis, PTL also induced G0/ G1 cell cycle arrest in a concentration- dependent manner in A549 cells and G2/M cell cycle arrest in H1792 cells (Additional file 1: Figure S1). The difference in cell cycle arrest induced in these two cell lines may be due to the p53 status [37, 38]. Collectively, these results show that PTL inhibits the growth of human lung cancer cells through induction of apoptosis and/or ADP ribosylation factor cell-cycle arrest. Figure 1 Parthenolide inhibits cell growth (A, B) and induces apoptosis in a concentration-dependent (C) and a time-dependent manner (D).

The indicated cell lines were seeded in 96-well plates and treated with the given concentration of PTL for 48 hrs. Cell survival was estimated using SRB assay (A) and MTT assay (B). Points: mean of four replicate determinations; bars: S.D. The indicated cells were treated with indicated concentrations of PTL for 24 hrs (C) or treated with 20 μmol/L PTL for various lengths of time and harvested for Western blot analysis (D). CF: cleaved form. Parthenolide triggers extrinsic apoptosis by up-regulation of TNFRSF10B expression In order to understand the molecular mechanism of PTL-induced apoptosis in NSCLC cell lines, several apoptosis-related proteins were examined. Data showed that TNFRSF10B was up-regulated after exposure to PTL (Figure 2A, B).

Herein, the high-frequency intercept with the X-axis represented the equivalent series resistance (R s), associated with the sum of the electrolyte BB-94 concentration solution resistance, the intrinsic resistance of active material, and the contact resistance at the electrode-electrolyte interface. The charge transfer resistance of electrode (Rct) was calculated from the diameter

of the semicircle in the high-frequency region, while the straight line at lower frequencies presented the diffusion behavior of ions in the electrode pores. The steeper shape of the sloped line represented an ideal capacitive behavior with the faster diffusion of ions in electrolyte [36]. The measured impedance spectra were analyzed using the complex nonlinear least-squares fitting method on the basis of the equivalent circuit, which is given in the inset of Figure  8d. From the magnified high-frequency regions in the inset of Figure  8d, the NCONAs electrodes after 1st and 3,000th cycles show the charge transfer resistances (R ct), respectively. The R ct value increases only slightly from 1st and 3,000th cycles owing to good contact between the current collector and nanoneedle arrays. These analyses revealed

that the good electrical conductivity and ion diffusion selleck chemical behavior resulted in the high performance of NCONAs selleck inhibitor carbon cloth composite as electrode material for SCs. Based on abundant electrochemical analysis, owing to the synergistic effects between nanoneedle arrays and carbon cloth, the flexible NCONAs and carbon cloth composite electrode material exhibit high specific capacitance. Florfenicol The improved electrochemical performance could be related to the following structural features. Firstly, large surface areas facilitate ion diffusion from the electrolyte to each NCONA, making full use of the active materials,

which undoubtedly contributes to the high capacitance. Secondly, carbon cloth in the hybrid materials could provide not only double layer capacitance to the overall energy storage but also fast electronic transfer channels to improve the electrochemical performances [29]. Third, the direct growth of NCONAs on a conductive substrate could ensure good mechanical adhesion, and more importantly, good electrical connection with the conductive substrate that also serves as the current collector in such binder-free electrodes [35, 37]. In this way, the decreased ion diffusion and charge transfer resistances lead to the improved specific capacitance. Meanwhile, the synergistic effects result in the better cycling stability of the NCONAs and carbon cloth composite electrode. NCONAs in a vertical array and carbon cloth as the platform for sustaining nanoneedles arrays withstand the strain relaxation and mechanical deformation, preventing the electrode materials from seriously swelling and shrinking during the insertion-deinsertion process of the counter ions [38, 39].

The clusters common and unique to the groups mentioned above are presented in additional file 3. In the BBH performed to all strains studied, 77 common genes were obtained, of which 17 (FixA, FixB, FixI, FixG, FixH, FixK, FixN, FixO, FixP, NifA, NifS, NodD, NodM, “”VirB234″”, VirG, TraG and TrbB) are related to biological nitrogen fixation and pathogenesis processes (Figure 2C).

Phylogenetic reconstructions were then performed to the proteins identified in the BBHs with more representativeness among the genomes analyzed. The topologies A-1210477 of Fix, Nif, Nod, Vir and Trb proteins (Figures 3 to 5, and additional file 4), have shown some incongruences when compared with the phylogeny model (Figure 1). The reconstruction obtained for FixNOP (Figure 3A) has a similar topology to the model with one exception. In the model reconstruction, Mesorhizobium BNC1 is close to the symbiont and pathogens branch, being grouped with M. loti, while in the FixNOP tree, Mesorhizobium BNC1 is distant from M. loti, in a highly reliable branch, suggesting that these genes in Mesorhizobium BNC1 could have originated from horizontal transfer. Figure 3 FixNOP, FixABC, TrbCFGIJ and FixS phylogenies. Phylogenies of selected

nitrogen fixation and conjugation proteins obtained by BBH, reconstructed with the Neighbor-Joining method of the Phylip 3.67 program, with 1,000 replicates for bootstrap support. (A) concatenated phylogeny for FixNOP proteins; (B) concatenated IWR-1 chemical structure phylogeny for FixABC proteins; (C) phylogeny for FixS protein; (D) concatenated phylogeny for TrbCFGIJ proteins. Figure 4 NodN and NodD phylogenies. Protein tyrosine phosphatase Phylogenies of Temsirolimus clinical trial selected nodulation proteins obtained by BBH, reconstructed with the Neighbor-Joining method of

the Phylip 3.67 program, with 1,000 replicates for bootstrap support. (A) phylogeny for NodN protein; (B) NodD protein. Figure 5 VirB 8 and VirB9 phylogenies. Phylogenies of selected proteins of type IV secretion system obtained by BBH reconstructed with the Neighbor-Joining method of the Phylip 3.67 program, with 1,000 replicates for bootstrap support. (A) phylogeny for VirB8 protein; (B) VirB9 protein. The phylogenetic tree obtained with FixABC (Figure 3B) was the most distinct from the phylogeny model. In the group of photosynthetic, methylotrophic and bioremediation bacteria, Azorhizobium caulinodans is close to Bradyrhizobium and distant from X. autotrophicus. In the pathogen and symbiont group, Rhizobium etli is grouped with M. loti and not with Rhizobium leguminosarum, which in turn is grouped with Ensifer (= Sinorhizobium)meliloti, while in the phylogeny model this bacterium is more related to M. loti. Interestingly, the same patterns of FixABC were obtained in NifAB, with the grouping of R. etli – M. loti and R. leguminosarum – E. meliloti (additional file 4). Furthermore, the grouping between R. etli and M. loti and the proximity between R. leguminosarum and E.

Proc Natl Acad Sci USA 2006, 103:19890–19895.PubMedCrossRef 36. Duan K, Dammel C, Stein

J, Rabin H, Surette MG: Modulation of Pseudomonas aeruginosa gene expression by host microflora through interspecies communication. Mol Microbiol 2003, 50:1477–1491.PubMedCrossRef 37. Sibley CD, Rabin H, Surette MG: Cystic Talazoparib price fibrosis: a polymicrobial infectious disease. Future Microbiol 2006, 1:53–61.PubMedCrossRef 38. Ryan RP, Fouhy Y, Garcia BF, Watt SA, Niehaus K, Yang L, Tolker-Nielsen T, Dow JM: Interspecies signalling via the Stenotrophomonas maltophilia diffusible signal factor influences biofilm formation and polymyxin tolerance Lonafarnib in Pseudomonas aeruginosa . Mol Microbiol 2008, 68:75–86.PubMedCrossRef 39. Senol E: Stenotrophomonas maltophilia : the significance and role as a nosocomial pathogen. J Hosp Infect 2004, 57:1–7.PubMedCrossRef 40. Looney WJ: Role of Stenotrophomonas maltophilia in hospital-acquired infection. Br J Biomed Sci 2005, 62:145–154.PubMed 41. Saiman L, Cacalano G, Prince A: Pseudomonas cepacia adherence to respiratory epithelial cells is enhanced by Pseudomonas Sapitinib order aeruginosa . Infect Immun 1990, 58:2578–2584.PubMed 42. Hoang TT, Karkhoff-Schweizer RR, Kutchma AJ, Schweizer HP: A broad-host-range Flp-FRT recombination system for site-specific excision of chromosomally-located DNA sequences:

application for isolation of unmarked Pseudomonas aeruginosa mutants. Gene 1998, 212:77–86.PubMedCrossRef 43. Christensen GD, Simpson WA, Younger JJ, Baddour LM, Barrett FF, Melton DM, Beachey EH: Adherence aminophylline of coagulase-negative staphylococci to plastic tissue

culture plates: a quantitative model for the adherence of staphylococci to medical devices. J Clin Microbiol 1985, 22:996–1006.PubMed 44. Rashid MH, Kornberg A: Inorganic polyphosphate is needed for swimming, swarming, and twitching motilities of Pseudomonas aeruginosa . Proc Natl Acad Sci USA 2000, 97:4885–4890.PubMedCrossRef Authors’ contributions APo, and PC performed the adhesion and biofilm formation assays on both polystyrene and IB3-1 cell monolayer. APo also carried out bacterial internalization assays, co-infection assays, motility tests, statistical analyses, and drafted the manuscript. VC took care of the additional experiments required during manuscript revision. MN and APe performed the construction of flagellar mutants. MN also participated in the revision of the manuscript. SG carried out microscopic analyses. EF and VS contributed by giving a medical point of view to the discussion of the results. EF also collected clinical strains used in the present work. RP, and GDB were involved in the design and coordination of the study, contributed to the revision of the manuscript, and gave their final approval of the version to be published.

Selective pressure mediated by the intensive use of antibiotics (both human and non-human) and several mechanisms for genetic transfer could have contributed to the rapid dispersal of antibiotic resistance in the community [1]. Antibiotics target both pathogenic bacteria as well as normal commensal flora, represented by skin, gut, and upper respiratory tract [2]. Current strategies to monitor the presence of antibiotic resistance in bacteria mainly rely upon examining resistance in pathogenic organisms and involve only periodic cross-sectional evaluations of resistance in the commensal

flora [3, 4]. Resistance see more amongst the commensal flora is a serious threat because a very highly populated ecosystem like the gut may at later stage be source of extra intestinal infection which may spread to other host or transfer genetic resistance element/s to other members of micro-biota including pathogens [5]. Despite this, there is paucity of data regarding the dynamics of antibiotic resistance in commensals. β-lactam antibiotics are the most commonly used antibiotics in community as well as hospitals. They are generally characterized by their favorable safety and tolerability profile as well as their broad spectrum activity [6]. The ever increasing variety of β-lactamases raises serious concern

about our dependence on β-lactam drugs. Rapidly emerging β-lactamases include diverse ESBL, Nirogacestat order AmpC β-lactamases, and carbapenem-hydrolyzing β-lactamases. ESBL producing Enterobacteriaceae were initially associated with nosocomial infections, however, recent studies indicate significant increase in the community isolates [7]. The risk posed by community circulation of the multidrug resistant bacteria is ISRIB nmr emphasized by the high concentration of ESBL in the community as well as the hospital onset intra-abdominal infections [8]. The rapid dissemination of ESBL’s in community may drive excessive use of carbapenems. The recent

report of Carbapenem resistance due to dissemination of NDM-1 β-lactamase producing bacteria Dapagliflozin in the environmental samples and key enteric pathogens in New Delhi, India may have serious health implications [9]. Several studies have been conducted to assess the risk factors associated with colonization and infection caused by ESBL producing Enterobacteriaceae, which include antibiotic use, travel, contact with healthcare system and chronic illness [10, 11]. Gut colonization in neonates with no direct antibiotic pressure were used as a model to evaluate β-lactam resistance in the community in absence of selection pressure. Methods Design overview, setting, and participants In this prospective study all low birth weight neonates (LBW) (≥1500 to <2500 g) born at the Safdarjung Hospital, New Delhi, India (2009–2011) were eligible and enrolled to study ‘Effect of Probiotic VSL#3 on prevention of sepsis during 0–2 month period’.

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