Although PEG remains the gold standard for the steric protection of liposomes [50], it creates an impermeable layer over the liposome surface [51] which could decrease availability of blood asparagines to encapsulated ASNase II. However, research in nanomedicine offers a unique platform for a variety of manipulations that can further enhance the value of the I-BET151 concentration delivered drugs. Conclusions It could be assumed by this study that, when the CSNPs are loaded with hydrophilic macromolecules or drugs, the interactions between them and the gel network can effectively make particles much more stable. The preparation of ASNase II-loaded CSNPs was based on an ionotropic interaction between the positively

charged CS and the negatively charged ASNase II and TPP. The negatively this website charged ASNase II was able to link CS chains electrostatically at pH ~ 5.7 before the addition of the polyanion. Such ASNase II behavior was previously observed in DEAE-Sepharose

column by positively charged amine groups of DEAE. ASNase II-CS interactions would be strengthened by adding a polyanion and rising pH. So, it could be assumed that CS networks were formed through two cross-linkers of TPP and ASNase II, and the drug itself helped particle formation that is of great interest in pharmaceutical productions. The pH and thermal stability, release, and half-life of ASNase II were evaluated. Compared to the free ASNase II, the immobilized enzyme was more resistant to alkaline pH (8.5 to 9.5) and to high temperatures. ASNase II release could be influenced by pH and the ionic strength of the medium. The immobilized enzyme had an increased half activity time of about 23 days in the low ionic strength solution and about

6.4 days in the high ionic strength solution. This in vitro study would provide an impetus for the future in vivo investigations. Further studies will be needed to find a suitable particle size and charge, biological responses, and administration route to apply in drug delivery and in vivo use. Acknowledgements We would like to thank the members of the Biotechnology Department of Razi Vaccine and Serum Research Institute for their help. This work was supported partly by Iran Nanotechnology Initiative Council and Hamadan University of Medical Sciences. Flavopiridol solubility dmso References 1. Narta UK, Thymidylate synthase Kanwar SS, Azmi W: Pharmacological and clinical evaluation of L-asparaginase in the treatment of leukemia. Crit Rev Oncol Hematol 2007, 61:208–221. 10.1016/j.critrevonc.2006.07.009CrossRef 2. Pasut G, Sergi M, Veronese FM: Anti-cancer PEG-enzymes: 30 years old, but still a current approach. Adv Drug Deliv Rev 2008, 60:69–78. 10.1016/j.addr.2007.04.018CrossRef 3. Wolf M, Wirth M, Pittner F, Gabor F: Stabilisation and determination of the biological activity of L-asparaginase in poly(D, L-lactide-co-glycolide) nanospheres. Int J Pharm 2003, 256:141–152. 10.

XAV939 Additional studies are warranted to provide support for the generalizability of these findings. Further, the sample sizes across studies are relatively small [19]. Thus, there is a high risk for confounding factors Cell Cycle inhibitor that may have skewed the data. For instance, an unmeasured characteristic of the men included within the present study like higher levels of the aromatase enzyme, may account for their lack of response to Resettin®.

Additional studies are warranted to more clearly delineate the association between Resettin® and serum testosterone levels. Findings from these studies are expected to improve the generalization of the conclusions. Notwithstanding, there was a measurable 38% GSK621 purchase increase in serum testosterone levels and a 4.5% decrease in estradiol among participants receiving the 1200 mg/day experimental group. Indeed, while this increase may not have reached the stringent criteria for statistical significance, this difference may be clinically relevant. Additional studies are warranted to

explore specific benefits to this degree of improvement in testosterone level. Moreover, given that serum DHT levels were significantly lower in both the 800 mg/day and 1200 mg/day treatment groups, and that Resettin®/MyTosterone™ has been shown to prevent the conversion of testosterone into DHT over time, it may be that this accounts for the rising testosterone levels in a subset of participants. Thus, additional studies that include a broader sample of study participants are warranted to explore for the generalizability of these findings. Future studies may also be needed to examine dosage level in relation to weight or BMI and androgen response. While weight specific dosing is not novel in terms of the pharmaceutical field, dietary supplements have not typically provided dosing instructions that are dependent upon the individual’s selleck chemical weight or BMI. It is expected that findings

from studies examining the impact of various dosages of Resettin®/MyTosterone™ on the metabolic profiles, specifically testosterone, DHT, and estrogen levels, across individuals who are overweight or obese will provide support for including weight dependent dosing instructions and, thus, improve the individual’s hormonal response to this natural dietary supplement. Additional studies are necessary to evaluate the full extent of the regulatory effects of Resettin® in the body’s efforts to resume homeostasis and return testosterone to ideal levels. This study highlights that there are likely ideal levels of testosterone in men. These data contribute to the possible benefits of using Resettin/Mytosterone for combating age-related androgen deficiency and andropause. Availability of supporting data There is no supporting data that is currently available. Acknowledgments M.L.A.

Inclusion of this indicator made it easier to

see the small recombinant colonies. Plates were seeded with 5 μl H. pylori liquid culture (forming a circle with 3 mm diameter) standardised to an OD600 nm of 1.0 and were incubated at 37°C for up to 7 days under the conditions described above. The motility halos were recorded using a digital camera and the area of each halo was measured using a GS-800 Calibrated Densitometer (Biorad). Motility analysis was also carried out by direct observation under phase-contrast microscopy using a Nikon Eclipse E600 after cells were grown in co-culture conditions as used by Wand et al. [24]. Briefly, co-cultures of H. pylori-human gastric adenocarcinoma (AGS) cells were prepared APR-246 mouse (described below). After 24 h, 10 μl culture was placed onto a microscope slide and covered with a coverslip and freely-motile H. pylori cells were analysed under the microscope. Plate motility bioassay using chemically defined media (CDM) The liquid chemically defined media were prepared as previously described [15, 28]. 60 ml of sterile chemically defined media were added to 40 ml of molten 1% Oxoid No. 1 agar base to make 0.4% semi-solid chemically defined agar. selleck kinase inhibitor cysteine supplemented

plates (CSP) were made by adding cysteine to the Sorafenib in vivo molten agar, shortly before it set. The final concentration of cysteine was 1.0 mM, which was non-limiting for H. pylori growth. The centre of each plate was seeded with one-day incubated H. pylori cells and was incubated for 5 Parvulin days under the conditions described above. The motility halos were recorded using a digital camera and the area of each halo was measured using a GS-800 Calibrated Densitometer (Biorad). Motility assay with AI-2 complementation AI-2 was synthesised enzymatically as described previously using purified proteins LuxS

E. coli and Pfs E. coli [8]. For complementation of the ΔluxS Hp motility phenotype, soft motility agar plates (0.4% w/v) were made as previously described. Bioluminescence activity of the AI-2 product was quantified using the V. harveyi bioassay and compared to CFS from H. pylori wild-type broth culture standardised to an OD600 nm of 1.0 at the time point in the growth curve that maximal AI-2 activity was measured. 1/400 diluted in vitro synthesised AI-2 product shows the same level of bioluminescence as seen in the H. pylori wild-type CFS in the V. harveyi bioassay. Therefore, in the complementation experiment AI-2 was added to motility plates to a final concentration of 0.25% (v/v). 24 h H. pylori cultures were seeded individually onto the centre of each motility plate and incubated for 5 days. The area of outward migration was recorded with a digital camera and measured using a GS-800 Calibrated Densitometer (Biorad). Tissue culture and bacterial co-culture All chemicals were obtained from Gibco, UK.

Br.013 group. One of the Georgian strains (F0673) was TGF-beta inhibitor sequenced using the Illumina Genome Analyzer II sequencing platform resulting in very high sequence coverage (averaging 1,076X) when aligned to the LVS genome (See Additional file 2, [26]). Subsequent whole genome sequence (WGS) comparisons among three published B.Br.013 group genomes (FSC 200, LVS, and RC503), the genome of strain F0673 generated for this study, and the published OSU18 genome (as an outgroup) revealed 650 putative SNPs. Most of these putative SNPs

(n = 470) were phylogenetically located on the branches separating OSU18 from the genomes in the B.Br.013 group (data not shown). Maximum parsimony analysis of the putative SNPs produced a phylogeny (Figure 1B)

with a very low homoplasy index (0.02), consistent with the highly clonal nature of F. tularensis. Bortezomib molecular weight The phylogenetic topology of the FSC 200, LVS, and RC503 genomes is consistent with previous publications [15, 16], and the small number of PXD101 price putative SNPs unique to the Georgian strain is consistent with the low genetic diversity observed among other lineages within F. tularensis subsp. holarctica [3, 6, 27, 28]. The new branch (B.Br.027) leading to the Georgian strain arises from a common ancestor that is basal to the previously described diversified lineages within the B.Br.013 group and is separated from them by only 45 putative SNPs, with 39 of these putative SNPs leading to the

Georgian strain (B.Br.027 in Figure 1B) and the other six putative SNPs along a branch (B.Br.026 in Figure 1B) defining a monophyletic lineage containing the other sequenced strains from this group. Identification of
ages and subclades We designed assays targeting 21 of the 39 putative SNPs leading to the sequenced Georgian strain (Table 1) and screened them across the 25 Georgian isolates (Table 2) to reveal additional phylogenetic structure among these strains. All 21 SNPs were determined to be real and assigned the 25 strains to a monophyletic lineage (B.Br.027; also referred to below as the Georgian lineage) that includes six new subclades (Figure 2A). We also designed an assay (Table Thymidine kinase 1) targeting one of six putative SNPs along the branch (B.Br.026 in Figure 1B) leading to the other sequenced strains (FSC 200, LVS, and RC503) and screened it across DNA extracts from these three sequenced strains, as well as the 25 strains in the Georgian lineage. Consistent with the bioinformatics analyses, DNA extracts from the three sequenced strains all possessed the derived state for this SNP, whereas the 25 strains in the Georgian lineage all possessed the ancestral state for this SNP. This confirmed that the SNP was real and also branch B.Br.026, which leads to the lineage that gave rise to the previously known subclades within the B.Br.013 group [16].

The contents of STX were determined with a commercial EIA specific for both STX1 and 2 in two-fold serial dilutions of the supernatants. check details For each antibiotic, in the upper part of the panel the OD of the STX-specific signal is click here plotted against the dilution of the supernatants. In the lower part of each panel, the STX-titers are

shown which were determined in the plots of the OD as indicated exemplarily for the 1x (green dashed lines) and 4x (red dashed lines) MIC of ciprofloxacin. Briefly, from the OD-value of the undiluted sample of the untreated culture a horizontal dashed line was drawn until it intersected the plot of a given MIC. From this intersection a vertical line was drawn to determine the dilution at which the OD-value of the respective supe rnatant equaled the OD-value of the untreated control. The inverse of this dilution was defined as the STX-titer of the sample. Shown are the means and standard errors of three independent experiments. Statistical significance is indicated by asterisks: * for p < 0.05; ** JNJ-26481585 for p < 0.01. Fosfomycin at subinhibitory

concentrations as well as at the 4x MIC increased the titers of STX of supernatants of strain O157:H7 up to 4-fold as compared to untreated controls, while fosfomycin did not significantly affect titers of STX2 in cultures of O104:H4 (Figure 2C). Fosfomycin has already been discussed as a risk factor increasing clinical symptoms in an outbreak of STEC O157:H7 among school children [9]. Our data document increased titers of shiga toxins in fosfomycin-treated cultures of STEC O157:H7 and, therefore, seem to support the conclusion not to treat patients infected with STEC O157:H7 with fosfomycin. However, fosfomycin does not induce the release of STX2 from STEC O104:H4 and treatment with 4x MIC even reduced STX2-titers. Thus, high doses of fosfomycin could be useful for the treatment of infections with STEC O104:H4. Gentamicin did not enhance the release of shiga toxin from either STEC O157:H7 or O104:H4 (Figure 2D). Rifampicin at gradually increasing concentrations in the range of 0.25x

to 4x MIC gradually increased the titers of STX released 4��8C by both STEC O157:H7 and O104:H4 up to 64-fold of untreated controls (Figure 2E). Chloramphenicol at 1x MIC in cultures of STEC O157:H7 increased titers about 4-fold, while a 4x MIC reduced titers below those of untreated controls (Figure 2F). In contrast, chloramphenicol at both the 1x and 4x MIC in cultures of STEC O104:H4 reduced the STX2 titers below those of untreated controls. The determination of STX2 by EIA does only reveal the amount of immunologically detectable STX2, which is not necessarily tantamount to intact and active toxin. Thus, in order to assess the impact of antibiotics, the release of active STX2 was determined in the supernatants of fluid phase cultures of STEC O157:H7 and O104:H4 by the classical cytotoxicity assay on Vero cells.

1994; Dobrikova et al. 2003); these bands are also associated with long tails outside the principal absorbance bands, which originate

from differential scattering of the left and right circularly Crenigacestat concentration polarized light (Garab 1996). Ψ-type bands correlate with the macro-organization of the main Chl a/b light selleck inhibitor harvesting complexes, e.g., in LHCII-only domains, as indicated by correlations between the intensity of these bands and the LHCII-content of the sample (e.g., Garab et al. 1991; Garab and Mustárdy 1999). The arrays of PSII-supercomplexes might also contribute to the Ψ-type CD signal. For example, in a mutant lacking one of the minor light-harvesting complexes, namely, CP24, the macro-organization of the PSII-supercomplexes is modified

as compared to WT. This results in the loss Selleck Nutlin3a of the main Ψ-type band in the red at around (+)690 nm (Kovács et al. 2006). The intensities of the Ψ-type CD bands between 660 and 700 (Fig. 1a) differ for WT and dgd1 thylakoids. These CD signals are shown to be determined by the long-range organization of the pigment–protein complexes, in particular LHCII (e.g., Garab et al. 1991; Garab and Mustárdy 1999) and PSII-supercomplexes (Kovács et al. 2006). Thus, the reduced intensity of the main Ψ-type CD bands (CD(685–703) and CD(685–671)) in the mutant (Fig. 1a) might either be due to a smaller size of the chiral macrodomains or to a different organization of the complexes affecting the learn more pigment–pigment

interactions. It should be noted that DGDG has been found to be required for the formation of ordered 3D crystals of LHCII (Nuβberger et al. 1993). Hence, our CD data strongly suggest that also in vivo in the thylakoid membranes DGDG modulates the macroorganization of the main light-harvesting complexes of PSII. As shown by Chl fluorescence lifetime measurements, alterations in the macroorganization in dgd1 affected only marginally the energy migration and trapping (Figs. 3, 4). The mutant exhibited a somewhat longer average Chl a fluorescence lifetime (Figs. 3f, 4). The assignment of the fluorescence lifetimes to particular protein complexes or macroassemblies is a rather complicated task for intact chloroplasts and isolated thylakoids, where a large variety of complexes and supercomplexes co-exist. For example, most studies on whole chloroplasts and intact thylakoid membranes suggested average values for the trapping time in PSII between ~300 and ~500 ps (e.g., Roelofs et al. 1992; Gilmore et al. 1996; Vasile’v et al. 1998). A very detailed study of the fluorescence kinetics of thylakoid membranes with varying composition was recently performed, using different combinations of excitation and detection wavelengths to assign the various lifetimes to PSI and PSII but this is not a trivial task (van Oort et al. 2010).

To increase the threshold of cowpea yields in Africa would require identification of genotypes that exhibit high symbiotic performance and better plant growth. Because cowpea nodulates freely

with both rhizobia and bradyrhizobia [1], it is often described as being promiscuous. Yet only few studies [1, 6–9] have examined the biodiversity of cowpea rhizobia and bradyrhizobia in Africa, the native home of this legume species. One study [6] reported four different Bradyrhizobium strains belonging to 3 genospecies, and concluded that the cowpea rhizobia appeared to be more diverse in arid areas. Recently, another study [8] grouped cowpea rhizobia from China into six genospecies, and linked microsymbiont distribution and diversity MG-132 mw to geographical location. Like most published reports on the biodiversity of selleck compound root-nodule bacteria, namely rhizobia,

bradyrhizobia, azorhizobia, sinorhizobia and mesorhizobia, none of the studies [1, 6–9] on cowpea rhizobia and bradyrhizobia has assessed the linkage between symbiotic functioning and bacterial IGS types resident in nodules and/or used for determining rhizobial biodiversity. Quantifying N2 fixation in legumes and linking amounts of N-fixed to the IGS types found in their root nodules, could provide some indication of the symbiotic efficiency of resident bacterial populations used for establishing rhizobial biodiversity. That way, studies of legume agronomy in the context of N contribution could add value to bacterial biodiversity and phylogeny in relation to symbiotic functioning. In this study, 9 cowpea genotypes were planted in field experiments in Botswana, South Africa and Ghana with the aim of i) trapping indigenous cowpea rhizobia in the 3 countries for isolation and molecular characterisation, ii) quantifying N-fixed in the cowpea

genotypes using the 15N natural abundance Methane monooxygenase technique, and iii) relating the levels of nodule functioning (i.e. N-fixed) to the IGS types found inside cowpea nodules, in order to assess strain IGS type symbiotic efficiency. Methods Experimental site descriptions In Ghana, the experiments were conducted at the Savanna Agricultural Research Institute (SARI) site at Dokpong, Wa, in 2005. The site is located in the Guinea savanna, (latitude 10° 03′ N, longitude 2° 30′ W, and altitude 370 m) and has a unimodal rainfall (1100 mm annual mean) that starts in May and ends in September/October. The soils are classified as Ferric Luvisols [10]. Prior to experimentation, the site had been fallowed for 3 years. In South Africa, the Agricultural Research Ricolinostat Council (ARC-Grain Crop Research Institute) farm at Taung, Potchefstroom, was used for the field trials. The Taung experimental site is located between latitudes 27° 30′ S and longitudes 24° 30′ E, and is situated in the grassland savanna with a unimodal rainfall (1061 mm annual mean) that begins in October and lasts until June/July the following year.

Comparisons of gene expressions via qPCR were performed by adopting the following primer designs: SOCS3 (5′-CAA ATG TTG CTT CCC CCT TA-3′ and 5′-ATC CTG GTG ACA TGC TCC TC-3′), SHIP1 (5′-TCC AGC AGT CTT CCT CAC CT-3′ and 5′-GCT TGG ACA CCA TGT TGA TG-3′), IRAK3 (5′-GGG TGC CTG TAG CAG AGA AG-3′

and 5′-ATC TGG AGG AGC CAG GAT TT-3′), AZD8931 SOCS1 (5′-CTG GGA TGC CGT GTT ATT TT-3′ and 5′-TAG GAG GTG CGA GTT CAG GT-3′), TOLLIP (5′-CCA CAG TGT GAG GGA TTG TG-3′ and 5′-TCT CCT TCT CAT GCC GTT CT-3′), MyD88 (5′-GCA CAT GGG CAC ATA CAG AC-3′ and 5′-GAC ATG GTT AGG CTC CCT CA-3′), IKKβ (5′-GCT GCA ACT GAT GCT GAT GT-3′ and 5′- TGT CAC AGG GTA GGT GTG GA-3′), TAK1 (5′-TTT GCT GGT CCT TTT CAT CC-3′ and 5′-TGC CCA AAC TCC AAA GA ATC-3′), TLR4 (5′-TGA GCA GTC GTG CTG GTA TC-3′ and 5′-CAG GGC TTT TCT GAG TCG TC-3′), IκBα (5′-GCA AAA TCC TGA CCA GGT GT-3′ and 5′-GCT CGT CCT CTG TGA ACT CC-3′), GAPDH (5′-GAG TCA ACG GAT TTG GTC GT-3′

and 5′-TTG ATT TTG GAG GGA TCT CG-3′), TRAF6 (5′-CTG CAA AGC CTG CAT CAT AA-3′ and 5′-GGG GAC AAT CCA TAA GAG CA-3′), IRAK1 (5′-GGG TCC AGG TGC TTC TTG TA-3′ and 5′-TGC TAG AGA CCT TGG CTG GT-3′). After reverse transcription of mRNA, 5 μl of the reverse transcription product were added to a BioRad iCyclerTM PCR system containing 0.3 μM of each primer. One-fold QuantiTect SYBR Green Nutlin-3a purchase PCR Master Mix was used as a fluorescent reporter (QuantiTect SYBR Green PCR, Qiagen). The condition was programmed as follows: (1) Denaturation at 94°C for 10 min; (2) Amplification for 40 cycles of denaturation at 94°C for 15 s, annealing at 55°C for 30 s, and extension at 72°C for 20 s. Cell viability assay 3-[4,5-dimethyl-2-thiazolyl]-2,5-diphenyl-2H-tetrazolium find more bromide (MTT) assay, which is based on the cleavage of the tetrazolium salt by mitochondrial dehydrogenases in viable cells. In order to determine toxicity concentration, approximately 105 cells were plated onto each well of 96-well plates for 24 h, followed by treatment

with different probiotic agents for 6, 8, 10, 12 and 14 hours. After incubation, 200 mL of MTT solution (0.5 mg/mL) were added to each well for 4 h after washing by PBS. Finally, the supernatant was removed and 200 μL of dimethyl sulphoxide (DMSO) were added to each well to dissolve the dark blue formazan crystals. The absorbance was measured by ELISA plate reader (Jupiter, ASYS Hitech, Austria) at 570 nm. To compare the results, the relative cell viability was GSK872 ic50 expressed as the mean percentage of viable cells compared with untreated cells (100%). Statistical analysis Each value is the mean of triplicate experiments in each group. Means comparison was carried out by Student’s t-test.

17 [1.73–5.82] 0.15   Nausea/vomiting 56 115.7/3,159.5 [3.7] 92.7/2,995.5 [3.1] 1.22 [0.92–1.61] 0.36   Abdominal pain 20 40.7/1,342 [3.0] 19.8/1,233 [1.6] 1.92 [1.12–3.27] 0.47 Aspirin SIS3 order vs. NSAIDs/analgesics  Gastrointestinal events 5 565/3,105 [18.2] 737/6,037 [12.2] 1.61 [1.43–1.82] 0.02  Minor gastrointestinal events 50 609.1/4,888 [12.5]

736.8/9,471 [7.8] 1.81 [1.61–2.04] 0.19   selleck chemical dyspepsia 26 233.9/3,889 [6.0] 258.3/7,427 [3.5] 1.94 [1.61–2.35] 0.43   Nausea/vomiting 43 206.5/4,693 [4.4] 320.4/9,229 [3.5] 1.37 [1.14–1.64] 0.17   Abdominal pain 20 369.6/3,755 [9.8] 406.9/7,332 [5.6] 1.95 [1.68–2.27] 0.42 Aspirin vs. ibuprofen  Gastrointestinal events 1 534/2,890 [18.5] 330/2,869 [11.5] 1.74 [1.50–2.02] SNX-5422 concentration ND  Minor gastrointestinal events 13 493.7/3,238 [15.2] 288.1/3,430 [8.4] 2.02 [1.73–2.37] 0.19   Dyspepsia 10 193.5/3,129 [6.2] 100.8/3,320 [3.0] 2.27 [1.76–2.93] 0.73   Nausea/vomiting 11 145.5/3,177 [4.6] 111.1/3,335 [3.3] 1.45 [1.13–1.87]

0.08   Abdominal pain 6 332.9/3,015 [11.0] 183.7/3,026 [6.1] 2.00 [1.65–2.42] 0.34 Aspirin vs. naproxen  Gastrointestinal events 0 ND ND ND ND  Minor gastrointestinal events 6 18.8/187 [10.1] 5.4/211 [2.6] 5.36 [1.95–14.7] 0.15   Dyspepsia 5 9.3/157 [5.9] 4.4/181 [2.4] 3.40 [1.03–11.2] 0.72   Nausea/vomiting 5

8.9/140 [6.3] 1/166 [0.6] 8.84 [1.54–50.8] 0.04   Abdominal pain 4 9.4/151 [6.2] 0/174 [0.0] 68.9 [0.93–5,100] 0.97 Aspirin vs. diclofenac  Gastrointestinal events 1 5/54 [9.3] 5/109 [4.6] 2.12 [0.59–7.67] Cediranib (AZD2171) ND  Minor gastrointestinal events 4 6.3/166 [3.8] 6.8/370 [1.8] 1.31 [0.39–4.46] 0.27   Dyspepsia 1 1/6 [16.7] 2.4/7 [34.3] 0.38 [0.03–5.45] ND   Nausea/vomiting 3 1/106 [0.9] 4/310 [1.3] 0.43 [0.04–4.95] 0.66   Abdominal pain 1 5/60 [8.3] 1/60 [1.7] 5.36 [0.61–47.4] ND CI confidence interval, ND no data, NSAID nonsteroidal anti-inflammatory drug, OR odds ratio a P value for heterogeneity In 59 studies with 3,304.5 subjects receiving aspirin and 3,170.5 subjects receiving placebo, 5.2 % of aspirin subjects reported a minor gastrointestinal complaint (abdominal pain, dyspepsia, or nausea/vomiting), versus 3.7 % of placebo subjects. The corresponding summary OR was 1.46 (95 % CI 1.15–1.86) [see Table 2 and see Appendix 3 in the Electronic Supplementary Material]. The ORs for dyspepsia (3.17, 95 % CI 1.73–5.82) and abdominal pain (1.92, 95 % CI 1.12–3.27) were also increased significantly. Similar findings emerged in comparisons of aspirin with any active comparator (50 studies with 4,888 and 9,471 subjects, respectively). The pooled risks of minor gastrointestinal complaints were 12.

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