Frontiers in Zoology 2006, 3:11 PubMedCrossRef 23 Ficetola GF, C

Frontiers in Zoology 2006, 3:11.PubMedCrossRef 23. Ficetola GF, Coissac E, Zundel S, Riaz T, Shehzad W, Bessière J, Taberlet P, Pompanon F: An In silico approach for the evaluation of DNA barcodes. BMC Genomics, in press. 24. Wu S, Mamber U: Agrep- a fast approximate pattern matching

tool. Proceedings of the Winter 1992 USENIX Conference San Francisco USA. Berkeley 1992, 153–162. 25. James T, et al.: Reconstructing the early evolution of Fungi using a six-gene phylogeny. Nature 2006, 443:818–822.PubMedCrossRef 26. SantaLucia JJ, Hicks D: The thermodynamics of DNA structural click here motifs. Annual Review of Biophysics and Biomolecular Structure 2004, 33:415–440.PubMedCrossRef 27. Duitama J, Kumar D, Hemphill E, Khan M, Mandoiu I, Nelson C: selleck screening library Primerhunter: a primer design tool for pcr-based virus subtype identification. Nucleic

Acids research 2009,37(8):2483–2492.PubMedCrossRef 28. Peay K, Kennedy P, Davies S, Tan S, Bruns T: Potential link between plant see more and fungal distributions in a dipterocarp rainforest: community and phylogenetic structure of tropical ectomycorrhizal fungi across a plant and soil ecotone. New Phytologist 2010, 185:529–542.PubMedCrossRef 29. Harris D: Can you bank on GenBank? Trends in Ecology and Evolution 2003,18(7):317–319.CrossRef 30. Landeweert R, Leeflang P, Kuyper T, Hoffland E, Rosling A, Wernars K, Smit E: Molecular identification of ectomycorrhizal mycelium in soil horizons. Applied and Environmental Microbiology 2003.,69(1): DOI: 10.1128/AEM.1169.1121.1327–1333.2003 31. Robinson C, Szaro T, Izzo A, Anderson I, Parkin P, Bruns T: Spatial distribution of fungal communities in a coastal graasland soil. Soil Biology and Biochemistry 2009, 41:414–416.CrossRef 32. Hong S, Bunge J, Leslin C, S J, Epstein S: Polymerase

chain reaction primers miss half of rRNA microbial diversity. The ISME shopping 2009, 3:1365–1373.CrossRef 33. Jeon S, Bunge J, Leslin C, Stoeck T, Hong S, Epstein S: Environmental rRNA inventories miss over half of protistan Selleckchem MG 132 diversity. BMC Microbiology 2008, 8:222.PubMedCrossRef 34. Sipos R, Szekely A, Palatinszky M, Revesz M, K M, Nikolausz M: Effect of primer mismatch annealing temperature and PCR cycle number on 16S rRNA gene -targetting bacterial community analysis. FEMS Microbiology Ecology 2007, 60:341–350.PubMedCrossRef 35. Engelbrektson A, Kunin V, Wrighton K, Zvenigorodsky N, Chen F, Ochman H, Hugenholtz P: Experimental factors affecting PCR-based estimates of microbial species richness and evenness. The International Society for Microbial Ecology Journal 2010. doi:10.1038/ismej.2009.153 36. Huber J, Morrison H, SM H, Neal P, Sogin M, Welch D: Effect of PCR amplicon size on assessments of clone library microbial diversity and community structure. Environmental Microbiology 2009,11(5):1292–1302.

Predicted ORFs are shaded according to their functional category

Predicted ORFs are shaded according to their functional category. Homologous ORFs are connected with lines. Prophage 06 and other prophage regions of P. fluorescens Pf-5 Prophage 06 is the largest prophage region of P. fluorescens Selleckchem Tozasertib Pf-5 and encodes a 56-kb temperate lambdoid phage integrated into tRNASer(see Additional file 4). It is mosaic in nature with no homologues present in strains Pf0-1 or SBW25. P. fluorescens Pf-5 carries four genomic copies of tRNASer, of which tRNASer(2) and tRNASer(3) are associated with prophages carrying integrases of different specifiCity (see Additional file 5). The anticodon, V- and T-loops of tRNASer(2) are

parts of the 104-bp putative attB site of prophage 06, whereas the T-loop of tRNASer(3) forms part of the 60-bp putative attachment site of prophage 02. The latter is a prophage remnant that spans 8.4 kb and consists

of a gene encoding an ATP-dependent nuclease (PFL_1842) and a phage integrase gene with two internal frameshift mutations (see Additional file 6). The mobility of prophage 06 probably is mediated by a lambda-type integrase encoded by PFL_3794, which resides adjacent to the putative attR site. Prophage 06 contains gene modules that are involved in head morphogenesis (capsid proteins PFL_3764 and PFL_3765), this website DNA packaging (terminase PFL_3766), DNA recombination (a NinG-like protein, PFL_3773 PJ34 HCl and a putative NHN-endonuclease, Orf1) and tail morphogenesis (tail tip fiber proteins PFL_3744 and PFL_3751, tail length tape measure protein PFL_3753, and minor tail proteins PFL_3749, PFL_3750, and PFL_3752). The tail

assembly module resembles the corresponding region from Burkholderia thailandensis bacteriophage φE125 [27], although in prophage 06 the module is split by the integration of four extra genes (Fig. 5B). Prophage 06 also contains a regulatory circuit with genes for a Cro/C1 repressor protein (PFL_3780) and two putative antirepressor proteins (PFL_3747 and PFL_3746); a gene for a putative cytosine C5-specific methylase (PFL_3792); and lysis genes encoding holin (PFL_3770) and endolysin (PFL_3798). However, since the endolysin gene is localized Go6983 beyond the putative attR site it is not clear whether it represents part of the prophage 06 genome or a remnant from integration of a different phage (see Additional file 4). Finally, prophage 06 contains two genes, PFL_3740 and PFL_3796, which probably arose through gene duplication and encode putative conserved phage-related proteins that are 88% identical to one another. Prophages 04 and 05 are prophage remnants with reduced size and/or complexity that carry several mutated phage-related genes (Tables 1, see Additional files 7 and 8). Prophage 04 (13.5-kb) has an average G+C content of 56.

jejuni and epithelial cells is capable of inducing pro-inflammato

jejuni and epithelial cells is capable of inducing pro-inflammatory and pro-secretory processes [8, 16]. These are associated with cellular invasion [17] and secretion of IL8 by CLDT dependent and independent mechanisms [16, 18]. Direct use of a BCE has allowed us to use a reductionist approach to investigate effects of C. jejuni that are not dominated by these linked processes of cellular invasion by live bacteria and by toxin based cell lysis. 3-Methyladenine clinical trial BCE

has been determined to contain polysaccharide and protein components of the cell. As demonstrated previously the NF-κB inducing activity of C. jejuni BCE is relatively insensitive to digestion by protease K [8]. However the protein content has been determined using tryptic digests of SDS-polyacryamide extracted protein bands using MALDI-TOF

mass spectrometry as flagellin (Cj1339c), trigger factor (Cj0193c), lipoprotein (Cj0983), major outer membrane protein (Cj0599), cytochrome-c peroxidase (Cj0358), bacterioferritin (Cj1534c), cell binding learn more factor PEB4A (Cj0496), hypothetical protein (Cj0706), periplasmic protein (Cj0772c), fibronectin binding protein (Cj1478c), non-heme iron protein (Cj0012c), periplasmic protein (Cj1380), periplasmic protein (Cj0420), periplasmic protein (Cj0998c), DNA-binding protein HU (Cj0913c), periplasmic cytochrome C (Cj1153) and thioredoxin (Cj0147c) [11]. The polysaccharide component features α-glucan oligomers. The C. jejuni extract is notably devoid of the dominating heat-labile effects of the CLDT. C. jejuni BCE, like infection with live C. jejuni, has been shown to be a potent inducer of NF-κB using either luciferase based reporter assays, western blots with antibodies against IκB or electrophoretic mobility shift assays in epithelial cells [8] but, unlike treatment with live C. jejuni, this does not lead to host cell lysis. These observations are consistent with the hypothesis that a heat stable component plays a significant role in the pro-inflammatory response upon exposure

to C. jejuni. We hypothesize that NF-κB modulation is central to the response Myosin of enterocytes to C. jejuni BCE; to study this we determined the global changes in gene expression induced by C. jejuni BCE treatment of the well-differentiated human colonocyte line HCA-7, clone 29. In order to ensure the relevance of our results we have adopted stringent criteria for the identification of significantly affected genes and used the IPA program to determine the functional links between these gene products, identify the signalling pathways and networks to which they belong. These changes were validated by showing similar affects on mRNA levels when genes of interest were investigated by real-time quantitative PCR. Consistent with the initial hypothesis that NF-κB plays a major role in the response of HCA-7 cells to C. jejuni BCE, and features in 8 of the 11 designated signalling pathways Selleckchem 4SC-202 identified by IPA as up-regulated.

61 0 34 8 82 0 15 0 83 Sucrose 1 51 0 46 13 10 0 13 0 68 Lactose

61 0.34 8.82 0.15 0.83 Sucrose 1.51 0.46 13.10 0.13 0.68 Lactose 1.35 0.24 8.00 0.15 0.89 Trehalose 1.50 0.43 9.21 0.12 0.74 Fructose 1.51 0.34 7.50 0.18 0.78 Dextrins 1.61 0.31 11.0 n.d. n.d. The concentration AZD1080 research buy of biomass and selleck kinase inhibitor lactic acid were measured in the broth after 24 h of growth. Yx/s indicates g of dry biomass produced per g of substrate; Yp/s indicates g of lactic acid produced per g of substrate; μ8h indicates the specific growth rate in h−1 calculated in the first

8 h of growth. Values are an average of 3 different experiments with standard deviations ≤ 5%. Batch and microfiltration fermentation processes Glucose and sucrose were selected as carbon sources for the following batch experiments. During these experiments L. crispatus L1 demonstrated a similar growth rate and final concentration of cells. The maximum titer of biomass on the two substrates was slightly different, in particular, 3.9 ± 0.2 gcdw∙l−1 were obtained on glucose and 3.4 ± 0.1 gcdw∙l−1 on sucrose eFT508 (Table 2). The final amount of lactic acid was also quite similar, and it corresponded to 12 and 14 g∙l−1 on glucose and sucrose, respectively. Product (lactate) inhibition was also studied to better characterize the physiology of L. crispatus L1. Increasing amounts of sodium lactate added to the SDM medium at a fixed pH lowered the initial specific growth rate (1–3 h). In particular, μ appeared to

be reduced by half with 45 g∙l−1 lactate (Figure 2). In order to dilute lactic acid and overcome inhibition Arachidonate 15-lipoxygenase problems, a bioreactor with microfiltration modules was used to perform in situ product removal experiments (Figure 3). A maximum of 27.1 gcdw∙l−1 in 45 h of growth were produced with a final

concentration of 46 g∙l−1 of lactic acid. As it is shown in Table 3, a 7-fold improvement of the final titer of biomass was achieved by microfiltration experiments compared to previous batch processes. Moreover the total amount of lactic acid produced was equal to 148 g (ϕ = 0.37 g∙l−1∙h−1) with a Yp/s of 0.75 g∙g−1 (Table 3). All results presented are average of at least 3 experiments. Table 2 Yield of biomass and lactic acid obtained in batch experiments of L. crispatus L1 grown on SDM supplemented with 20 g · l −1 glucose or sucrose as main carbon sources Carbon source Cell dry weight (g · l−1) Lactic acid (g · l−1) μmax(h−1) Glucose 3.8 ± 0.3 11.5 ± 0.5 0.84 Sucrose 3.3 ± 0.2 13.6 ± 0.4 0.60 The medium contained soy peptone and yeast extract as nitrogen sources. Figure 2 Lactate inhibition curve. The graph shows the specific growth rate of L. crispatus L1 using increasing concentrations of sodium lactate in the medium at pH 6.5. Figure 3 Growth of L. crispatus L1 in a microfiltration experiment. Time course of biomass, production of lactic acid and residual glucose on SDM.

CagA has been associated with both stimulation

and inhibi

CagA has been associated with both stimulation

and inhibition of apoptosis [11, 12, 34]. Biliary cells exposed to cagA + H. pylori at a very low inoculum (MOI 1:1) demonstrated increased cell growth, whereas at MOI of 200:1, apoptosis was stimulated [35]. CagA may even directly antagonize the pro-apoptotic effect of VacA, as seen in AGS cells [31]. Apoptosis occurs after a number this website of cellular events, leading to activation of caspase-3, which is thought to constitute the basic effector of apoptosis. In the present study, both inhibitory and stimulatory genes showed significant differential expression, demonstrating the complexity of the influence of H. pylori on apoptosis: caspase inhibitors HSPA5 and DHCR24 showed similar late down-regulation as heat shock genes HSPA1B, HSPB1, which are also associated with apoptosis stimulation (cluster E, Table 3). On the other hand, TNFAIP3, BIRC2, BIRC3 and SERPINB2,

also associated with apoptosis inhibition, demonstrated early and persistent selleck compound up-regulation grouped together in cluster A. However, positive regulators of apoptosis PTPRH, TNFRSF12A, IL24, GADD45A, TRIB3, DDIT4, PHLDA4, Bucladesine order PP1R15A and SQSTM1 were all up-regulated in similar pattern after 6-12 h (cluster C). MCL1, an anti-apoptotic gene expressed in response to CagA injection [11], demonstrated increasing up-regulation over the course of the study. There were no significant changes in BCL-2 and very Evodiamine little increase in BAX expression in our study, two important genes that determine the sensitivity of cells to other apoptotic stimuli [36–39].

Noteworthy, there was marked up-regulation of TP53BP2, an important tumor suppressor gene (TSG) in human cancer, primarily stimulating p53 promotion of apoptosis genes. On the other hand, TP53BP2 is coding ASPP2 protein, which has also been shown to stimulate apoptosis independently of p53 [40–42]. However, Buti et al. recently demonstrated that CagA injected into gastric epithelial cells targeted ASPP2 protein to inhibit p53-mediated apoptosis [12]. The increased TP53BP2 expression seen in our study, might therefore potentiate this effect by increasing the CagA-ASPP2 interaction to cause increased inhibition of p53-mediated apoptosis. In fact, the current study showed that p53 target genes involved in apoptosis [43] such as FAS, DR4, TNFRSF10B (also referred to as DR5/KILLER), DCR1, DCR2, P53AIP1, CASP6, APAF1 and BNIP3L did not show any significant increase, and BNIP3L, CASP6 and APAF1, BID and BAX showed only little increase. p53 target genes regulating non-apoptotic cellular processes including MDM2, GADD45A, CDKN1A (also known as P21 WAF1/CIP1), EGFR, CCND1, CCNG2 and TGFA demonstrated moderate to marked up-regulation. This differential gene expression identified among the p53 target genes in this study, may indicate selective inhibition of p53-mediated apoptosis due to increased CagA-ASPP2 interaction, consistent with Buti’s findings.

By the late Holocene, when climate favoured succession of oak sav

By the late Holocene, when climate favoured succession of oak savannah to forest, many generations of people over thousands of years would have observed the role and importance of fire in maintaining savannah and woodland structure. Historical accounts indicate that Garry oak ecosystems were ignited in late summer and fall (Boyd 1986; Fuchs 2001; Turner 1999). By the mid-1800s, however, selleckchem as Europeans began clearing portions of southeastern Vancouver Island for agriculture, large fires were commonly observed (Grant 1857; Maslovat 2002). It is unclear whether the constant veil of summer smoke reported

during this time originated from lightning strikes, from fires lit by aboriginal peoples, or from the settlers themselves who burned for cultivation and after logging. Europeans restricted cultural burning in southwestern BC through the Bush Fire Act of 1874 (MacDonald 1929). In less than 100 years, European settlement, followed by fire exclusion, disrupted the fire regime in virtually all western North American oak ecosystems that have been studied (Pyne 1982). Palaeoecological context Early to mid-Holocene The Holocene climate along south coastal British Columbia has varied considerably over the last 12,000 years (Mathewes 1985;Hebda 1995; Walker and Pellatt 2003). After deglaciation, warm dry conditions occurred on southeastern Vancouver Selleck RG7112 Island (11,450–8,300 BP) and were typical of climate throughout the coast

of BC at the time (Walker and Pellatt 2003), with frequent fires also occurring in the Fraser Valley (Mathewes 1973). These conditions supported Douglas-fir (Pseudotsuga menziesii) parkland with abundant grasses (Poaceae) and bracken fern (Pterdium) (Pellatt et al. 2001) (Fig. 2). These and other species present in the pollen record indicate a relatively warm/dry climate with frequent disturbance, likely fire. Garry oak arrives curiously late along the south BC coast (~8300 BP), HSP90 but quickly increases in abundance after its arrival (Allen 1995; Heusser 1983; Pellatt et al. 2001). Although

maximum summer temperature for the Holocene occurred between 11,000 to ~8000 BP (Mathewes and Heusser 1981; Rosenberg et al. 2004), oak pollen was rare prior to 8300 BP and peaked at 8000 BP or later on southern Vancouver Island (Allen 1995; Heusser 1983; Pellatt et al. 2001). A slow northward migration across the southern Gulf Islands to Vancouver Island, and thus, a long time lag following climatic change, offers a possible explanation for this species’ late arrival. Fig. 2 Simplified Pollen Accumulation Rate (grains/cm/year) Diagram from Saanich Inlet, BC. Red (Zones 1a and 1b) represents conditions that are warmer, dryer and more continental than present, yellow (Zone 2) is warmer and wetter, green (Zone 3) is a transitional cooling phase, and blue (Zone 4a and 4b) represents the establishment of conditions more typical of the present day.

Identical residues are marked with an asterisk (*) #

Identical residues are marked with an asterisk (*). Bucladesine Dashes represent

gaps introduced to preserve alignment. Conserved catalytic residues are indicated in boxes. The trees inferred by the maximum parsimony (MP) and neighbor-joining (NJ) methods showed less resolution than those built by Bayesian analysis, as they had a number of unresolved branches. The general topology obtained is Obeticholic represented by the Bayesian 50% majority rule consensus tree, in which the Bayesian posterior probabilities, MP and NJ bootstrap support are indicated on the branches (Figure 5). Figure 5 Phylogenetic tree of pectin lyases. The phylogeny shown is the Bayesian topology and branch lengths inferred using MrBayes vs. 3.1.2, with the Blosum 62 + G model. Numbers above the diagonal indicate posterior probability values from Bayesian analysis. Numbers below the diagonal indicate bootstrap percentage values from a bootstrap analysis inferred using the same alignment with PAUP*4.0 and Neighbor-J, respectively. A. thaliana pectate lyase was used as an outgroup. The asterisks represent branches that were not supported in 50% or more of the Daporinad solubility dmso bootstraps. The scale bar represents the number of substitutions per site. The phylogenetic tree was

edited using Dendroscope software [77]. Bayesian analysis allowed the separation of pectin lyases into two groups: one representing bacteria with 100% posterior probability and 100% bootstrap support for MP and NJ analysis, and the other one representing fungi and oomycetes with 100% posterior probability and 98% old bootstrap support for NJ. In the group formed by bacteria, sequences from Pectobacterium atrosepticum, P. carotovorum and Bacillus subtilis cluster together with 100% posterior probability. This early separation

between amino acid sequences of bacteria and those of oomycetes and fungi can be explained in terms of the evolution of lytic enzymes in these microorganisms for different purposes. Bacteria and some anaerobic fungi produce multi-enzymatic complexes called cellulosomes, which are anchored to the cell surface, allow the microorganisms to bind to lignocellulose substrates and increase the breakdown efficiency of cellulose, hemicellulose and pectin [62, 63]. In contrast, in the majority of fungi and oomycetes, cellulases, pectinases and hemicellulases are not integrated in cellulosome complexes, and the pectin degradation is regulated by a multifunctional control system in which the enzymes act in a synergistic manner and are induced by monosaccharides or small oligosaccharides that are generated as products of the same enzymatic reactions [64, 65]. The inferred tree also showed that the analyzed sequences of saprophytic/opportunistic fungi are clustered into a monophyletic group with 98% posterior probability and 75% and 70% bootstrap support for MP and NJ analyses, respectively.

Jpn J Geriat 1997, 34:298–304 CrossRef 10 Pan X, Wu T, Zhang L,

Jpn J Geriat 1997, 34:298–304.CrossRef 10. Pan X, Wu T, Zhang L, Song Z, Tang H, Zhao Z: In vitro evaluation on adherence and antimicrobial properties of a candidate probiotic Clostridium butyricum CB2 for farmed fish. J Appl Microbiol

2008, 105:1623–1629.PubMedCrossRef 11. Li YY, Chang JW, Hsieh LL, Yeh KY: Neutralization of interleukin (IL)-10 released by monocytes/macrophages enhances the up-regulatory effect of monocyte/macrophage-derived IL-6 on expressions of IL-6 and MUC1, and migration in HT-29 colon cancer cells. Cell Immunol 2010,265(2):164–171.PubMedCrossRef Selleckchem ATM Kinase Inhibitor 12. Wang JB, Qi LL, Zheng SD, Wang HZ, Wu TX: Curcumin suppresses PPARδ expression and related genes in HT-29 cells. World J Gastroenterol 2009, 15:1346–1352.PubMedCrossRef 13. Jin S, Zhang QY, Kang XM, Wang JX, Zhao WH: Daidzein induces MCF-7 breast cancer cell apoptosis via the mitochondrial pathway.

Ann Oncol 2010, 21:263–268.PubMedCrossRef 14. Jia YD, Lin JX, Mi YL, Zhang CQ: Quercetin attenuates cadmium-induced oxidative damage and apoptosis in granulosa cells Capmatinib manufacturer from chicken ovarian follicles. Reprod Toxicol 2011,31(4):477–485.PubMedCrossRef 15. Christensen HR, Frøkiaer H, Pestka JJ: Lactobacilli differentially modulate expression of cytokines and maturation surface markers in murine dendritic cells. J Immunol 2002,168(1):171–178.PubMed 16. Altonsy MO, Andrews SC, Tuohy KM: Differential induction of apoptosis in human colonic carcinoma cells (Caco-2) by Atopobium, and commensal, probiotic and enteropathogenic bacteria: mediation by the mitochondrial pathway. Int J Food Microbiol 2010,137(2–3):190–203.PubMedCrossRef 17. Zhang WJ, Li BH, Yang XZ, Li PD, Yuan Q, Liu XH, Xu SB, Zhang Y, Yuan J, Gerhard GS, Masker KK, Dong C, Koltun WA, Chorney MJ: IL-4-induced Stat6 activities affect apoptosis and gene expression these in breast cancer cells. Cytokine 2008,42(1):39.PubMedCrossRef 18. Fiorentino DF, Zlotnik A, Mosmann TR, Howard M, O’Garra A: IL-10 inhibits cytokine

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The most common presenting symptoms were abdominal pain (29%), bo

The most common presenting symptoms were abdominal pain (29%), bowel habit change (26%) and lower gastrointestinal bleeding (26%). Decreased stool frequency was the predominating symptom in 19 cases (6%). Other pathological parameters and their association with survival are presented in Table1. The average waiting time from the first hospital visit to the operation was 35 days. Table 1 Selected demographic and medical parameters and their association with 5-year overall survival (OS) and modes of surgery     Survival probability Emergency

surgery Parameter No. (cases) (%) 5-year OS (%) Log-rank p-value (cases) (%) p-value All 329 64.1 – 22 (7) – Sex AZD1480     0.5   0.73 male 191 (58) 62.4   12 (6)   Selleck Momelotinib female 138 (42) see more 66.5   10 (7)   Age     0.51   0.35 < 60 years 136 (41) 66.7   7 (5)   ≥ 60 years 193 (59) 62.3   15 (8)   Co-morbidity     0.71   0.97 Absent 193 (59) 65.5   13 (7)   Present 136 (41) 61.7   9 (7)   Serum CEA     < 0.01   0.32 < 5 ng/ml 144 (59) 71.1   8 (6)   ≥ 5 ng/ml

102 (41) 54.8   9 (9)   Tumor site     0.32   0.79 Rectum 94 (29) 56.8   5 (5)   Colon 223 (68) 66.8   16 (7)   T     0.02   0.18 T0-2 47 (14) 75.9   1 (2)   T3-4 282 (86) 62   22 (8)   N     < 0.01   0.34 N0 171 (53) 78.7   9 (5)   N1-2 152 (47) 49.4   12 (8)   M     < 0.01   0.02 M0 281 (85) 72.1   15 (5)   M1 48 (15) 18.5   7 (15)   Tumor differentiation     0.16   0.77 Well/Moderate 279 (92) 64.9   18 (7)   Poor 25 (8) 58.6   2 (8)   Lymphovascular invasion     < 0.01   0.12 Absent 276 (84) 69   16 (6)   Present 51 (16) 35.3   6 (12)   Lymph node ratio     < 0.01   0.53 < 0.35 273 (86) 72.7   17 (6)   ≥ 0.35 46 (14) 23.6   4 (9)   Endoscopic obstruction     0.73   < 0.01 Absent 120 (37) 67.2   2(2)   Present 209 (64) 62.3   20 (10)   Mode of operation     < 0.01   - Elective 307 (93) 66.4   -   Emergency 22 (7) 32.3   -   CEA carcinoembryonic antigen. Endoscopic

obstruction and factors associated with this finding On colonoscopy, the endoscope could not be passed beyond the tumor mass in 209 cases (63%). Clinical symptoms suggestive of early obstruction including decreased stool frequency or change in bowel habit were not significantly correlated with eOB (p-values 0.64 and 0.45, respectively). Although a primary tumor situated at the right colon had a significantly lower incidence of predominating obstructive symptoms (1%) than a left-sided Tobramycin CRC (8%) (p-value 0.02), the right-sided tumors had a higher incidence of eOB (72%) when compared to those on the left (60%, p-value 0.047). Colonic tumors had a higher incidence of eOB (70%) than rectal tumors (50%) (p-value < 0.01). Considering tumor size, CRC with eOB had a significantly larger size (5.9 cm compared with 5.2 cm, p-value < 0.01) and a higher frequency of T3-4 lesions (91% compared to 75%, p-value < 0.01). Also, eOBs were associated with lower serum albumin level (3.7 g/dl, compared to 3.9 g/dl, p-value 0.04) and lower hemoglobin level (10.5 g/dl, compared to 11.2 g/dl, p-value < 0.01) (Table 2).

Med Sci Sports Exerc 2000, 32 (3) : 654–658 PubMedCrossRef 6 Can

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