In contrast to that, Viikari-Juntura et al. (1996) reported an increased risk of EPZ5676 solubility dmso reporting high workload for forest industry workers having severe low back pain, e.g. for kneeling and squatting (OR, 1.6; 95 % CI, 1.2–1.9). Again, sample size was small (18 subjects with and 18 subjects without low back pain), and squatting or kneeling was rare in both groups (median, 0.0 h each). As the present study has dealt with knee complaints, our results cannot be closely compared to those studies. Moreover, our study concentrated on kneeling or squatting tasks (median, 32.7 min

or 29.7 % (0.0–92.7) of knee postures per measurement). With certain constraints, it should be noted that subjects with severe knee pain probably did not participate in our study due to sick leave. Study limitations The present study has several limitations that should be considered when interpreting the results. The study was based on the voluntariness of participation of companies and subjects, which might have

led to selection bias. Moreover, we examined only tasks where we expected knee-straining postures. Thus, our results are not representative for the whole working content of the examined trades. While in survey t 0 all measured subjects filled out the questionnaire, in survey t 1, only 65.8 % of the participants responded. However, compared to response-rates of other studies in Germany, this can be seen as click here quite successful (Latza et al. 2004). A non-responder analysis yielded similar to identical characteristics for responders and non-responders (see Appendix B in Supplementary Material). This lack of difference suggests that the lost to follow-up may not be an important issue, and the risk of a non-responder bias may be ruled out. As the second survey was conducted by mail, study participants were only able Teicoplanin to ask comprehension questions in the first survey when study staff was on site. Thus, comprehension problems

may have occurred in the second survey more often and may have biased the exposure see more assessment, for example by self-reported exposure wrongly related to a whole work shift, rather than to the measuring period. However, we attempted to minimise this effect by using the same questionnaire as in the first survey, accompanied by information on how to correctly fill it out. In addition, we gave a short description of the work performed during the exposure measurement at t 0. This procedure could have artificially reduced recall bias as such information cannot be provided in an epidemiological study, for example. Our survey covered a pre- and post-period of 6 months, while in reality, there are mostly several years or decades between exposure and retrospective assessment.

A dynA ezrA double deletion leads to a strongly exacerbated phenotype in cell division, suggesting that like EzrA, a regulator

of FtsZ ring formation, B. subtilis dynamin affects an early stage in cell division. However, the combination of a dynA deletion with a divIB deletion also leads to a synthetic effect on cell division. DivIB affects a state in division clearly later than the formation of the Z ring, indicating that the function of DynA in division cannot be correlated with a defined stage in division. In any event, the accumulation of dynamin at the Z ring underlines the idea that dynamin confers a function during division. Expression of DynA in a eukaryotic cell system showed that the protein has intrinsic affinity to the cell membrane Fer-1 in vitro and can assemble into tubulated PKC412 chemical structure structures. However,

these pointed outwards of the cells, while the assumed function of dynamin in the bacterial cell would either be an inward bending of the membrane during cell division, or the fusion of membranes as the last step during division. It is likely that DynA needs cofactors for its appropriate function in the bacterium. Interestingly, the combination of a dynA deletion with the deletion of a gene encoding for a flotillin-like protein, FloT, also leads to a synthetic defect in cell division. Flotillin proteins are implicated in lipid raft formation in eukaryotic and in prokaryotic cells. Although our experiments do not allow Pyruvate dehydrogenase us to make any clear conclusion as to the detailed function of dynamin or flotillin, they show that bacterial dynamin and flotillin proteins play non-redundant functions in membrane dynamics. This is supported

by our findings that each mutation does not affect the localization of the other protein. We suggest that dynamin is see more important for the generation of cell curvature, possibly via its putative mechanochemical activity, and likewise flotillin proteins, which may be important to recruit lipids that favour membrane bending. Indeed, there appears to be a link between flotillin in B. subtilis and membrane fluidity [37]. This idea is supported by our finding that DynA can distort the cell membrane in a heterologous cell system, suggesting that DynA may facilitate membrane invagination and/or couple Z-ring formation with membrane invagination. Alternatively, flotillin may be important to facilitate the recruitment of cell division proteins to the Z ring. In any event, the role of dynamin and flotillins in cell division is not redundant, because of the synthetic effect, and because of their different localization patterns.

The victims in our sample were those who chose to consult with the unit for advice and assistance as well as to document the violence in a manner than could be used to support legal process. Most victims learn more came through the emergency room of the hospital after receiving medical care. This population therefore could represent the “tip of the iceberg” of the most serious situations, i.e., those that required medical attention. Besides, people who seek medical attention in private practice are not systematically referred

to the Violence Medical Unit. Our relative small sample size limits the power of the statistical findings which should also be viewed in relation to a possible type I error given the number of tests performed. Finally, although we did not notice significant statistical differences

based on socio-demographic characteristics between the source population and the respondents to the telephone survey, we note that approximately half of the workplace violence victims could not be reached for follow-up. In conclusion, we believe our study shows the relevance and need for further RAD001 research on workplace violence victims, especially through longitudinal designs and a combination of quantitative and qualitative methods. There is a need to GKT137831 cell line verify in larger samples the initial psychological impact on victims of workplace violence, especially in a variety of occupations. Furthermore, the moderating effect of employer support deserves further investigation. Our findings suggest the need for employer responsiveness

and policies to reduce the impact and costs of workplace violence for society, organizations and victims. Acknowledgments We would like to thank the Groupe Progrès of the Swiss occupational accident insurance (Suva) who supported and funded this project. We are grateful to Dr. Patrick Gomez of the Institute for Work and Health for his valuable advice and comments on the first drafts Unoprostone of this article, and to Mr. Gilbert Leistner for his editorial advice. Conflict of interest The authors declare that they have no conflict of interest. Open AccessThis article is distributed under the terms of the Creative Commons Attribution License which permits any use, distribution, and reproduction in any medium, provided the original author(s) and the source are credited. Appendix 1: The six sections of the patient’s file 1. General data: gender, age, contact information (address, phone numbers), family doctor   2. Socio-demographic data: nationality, marital status, education level and occupation   3. Data concerning the violent event that motivated the consultation: date, time and place. Information on the perpetrator(s): number, gender, known/unknown by the victim; nature of the assaults (physical, sexual, psychological violence, deprivation or neglect), threats, complaint filed or intention to do so.   4.

NormFinder also enables estimation of the variation between sample subgroups, like

tumour and normal tissue, thus this algorithm can account for heterogeneity in the tested samples, which may be important considering the heterogeneity of the samples studied. The optimal normalization will vary with study design. The most suitable reference gene in one medical condition may be regulated in Gemcitabine mouse other tissues or diseases. Blanquicett et al., 2002, found that 18S, S9 and GUS were the least regulated genes among 15 putative reference genes when examining tumour and normal colorectal and liver tissues [28]. Furthermore, Dydensborg et al., 2006, identified B2M as the most appropriate gene for normalizing

colon carcinomas comparing to normal mucosa when they investigated seven colon adenocarcinomas containing both epithelial and stromal cells [29]. B2M was in this study identified as the least stable gene using NormFinder, and the third most variable gene using geNorm. In the present study where the tumour tissue samples consisted of more than 70% tumour cells some of the stromal cells are excluded. This might explain the discrepancies in the ranking of B2M since tumour tissue is heterogeneous and the fraction of INCB28060 manufacturer different cells may influence the gene expression results. Moreover, different patient groups, including age and clinical background, may also give dissimilarities across studies. CDK inhibitor Experimental variations may also influence the gene expression results, though using triplicates in the qRT-PCR analysis as used in this study will diminish this variation. Single assays qRT-PCR are time- and labour-intensive, 4��8C and require relatively large amounts of cDNA and PCR reagents in multivariate gene expression studies. TLDA overcome these drawbacks since this technique allows for simultaneously detection of expression of up to 384 genes and requires less template cDNA and PCR reagents than routine qRT-PCR [1, 31, 38–40]. Conclusions In this study we applied TaqMan Low Density Array in order to identify reference genes in

metastatic and non-metastatic colon cancer. The genes often used for normalization of gene expression data may be unstable and thus not suited for use, and therefore identifying stable reference genes in the specific experiment is vital for the results. The approach described herein can serve as a template to identify valid reference genes in any disease state. However, the optimal statistical approach to identify the best reference gene(s) remains to be determined. In the present study NormFinder and geNorm identified two different pairs of the most stable genes. The use of CTCV% might be a good validation of the two results. Nevertheless, the expression of target genes should be evaluated and a comparison of the effect of each pair of reference genes should be determined.

Figure  5 shows the removal ratio of Rh.B with increasing loading check details amount of absorbent under visible-light irradiation recorded at 270 min. For the G/M-CdS, the photodegradation ratio of Rh.B keep increasing from 4 to selleck 20 mg, after which it

keeps constant; for CdS MPs, the photodegradation ratio of Rh.B gets to maximum at 30 mg. This is consistent with the result of adsorption-desorption equilibrium experiment, and the suitable loading amount of the G/M-CdS composites should be 20 mg in this work. Figure 4 Removal ratio of G/M-CdS and pure CdS MPs with increasing stirring time under visible-light irradiation. The loading amount of both materials is 20 mg. Figure 5 Removal ratio of G/M-CdS and pure CdS MPs with increasing loading amount under visible-light irradiation. The adsorption characteristics of the G/M-CdS composites are displayed Cell Cycle inhibitor in Figure  6. It can be seen that, after stirring the mixture of the G/M-CdS composites and Rh.B aqueous solution (Figure  6, left) under visible-light irradiation for 270 min, the supernatant turned nearly colorless (Figure  6, right). This proved that the G/M-CdS composites possessed the properties of adsorption capacity and photodegradation. We would like to attribute the high efficient photodegradation activity to the

electron transfer from CdS to graphene. As shown in Figure  7, CdS can be excited by UV light to generate electrons and holes. Then, the photogenerated electrons transfer to graphene while holes are left behind in CdS since the conduction band of CdS is more negative. This electron transfer route reduces the possibility of recombination of electron-hole pairs and prolongs the lifetime of charge carriers. In other words, the transfer of photoexcited electrons from CdS to graphene check facilitates the charge separation, producing more –OH responsible for photodegradation of Rh.B. Previous reports on graphene-CdS

composites as the adsorbent for the extraction of organic pollutants were mainly focused on nanoscaled CdS particles. Herein, the adsorption performance and photocatalytic activity of the large-sized CdS/G composite with approximately 0.64 μm CdS particles were investigated, and the results exhibited that the current composites possess comparable purification ability of waste water with that of nanoscaled CdS/graphene composites. The accurate decision of size effect of large CdS particles needs further investigation, which is a subject of our future research. Figure 6 Rh.B solution (0.01 mg/mL, left) before and after separation of G/M-CdS adsorbent after photodegradation (right). Figure 7 Illustration of charge separation and transfer in G/M-CdS system. Conclusions In summary, we have successfully prepared G/M-CdS composites via an effective solvothermal method. Their ability of extraction of dye from aqueous solution was examined using Rh.B as adsorbate.

5% of the DNA was mutated. Table 3 GSK461364 Comparison of EGFR status (wild type (WT) or mutant (M)) of exon 19 and exon 21 determined by big dye sequencing or by pyrosequencing

on 58 NSCLC tissues Exon 19   big dye sequencing Exon 21   big dye sequencing     WT M     WT M pyrosequencing WT 47 / pyrosequencing WT 53 /   M 2 9   M 1 4 We then determined the EGFR status of 213 patients with advanced or metastatic lung adenocarcinomas for selection of to anti EGFR therapies (table 4). click here Seven (3.3%) samples were inconclusive due to poor DNA quality with no DNA amplification. Of the 206 remaining samples, 18 EGFR mutations were detected (8 of exon 19 and 10 of exon 21) (18/206; 8.7%). Among these 206 specimens, 36 had less than 20% of tumor cells and only one with a mutation was detected (1/36; 2.8%). For the 170 specimens containing more than 20% of tumor cells, 17 with mutations were found (17/170; 10%). Table 4 Prospective evaluation of the Lenvatinib mouse EGFR status of exons 19 and 21 % of tumoral tumoral samples (n = 206) EGFR mutations (n = 18)   cells number

% exon 19 exon 21 % <20% 36 17.5 0 1 2.8 from 20 to 50% 98 47.6 3 6 9.2 >50% 72 35 5 3 11.1 Samples may contain at least 20% of tumor cells to allow a correct detection of mutations Discussion Pyrosequencing is sensitive and enables accurate detection of mutations. A previous study has described the capacity of this method to detect small insertions [9] but this study is the first to demonstrate the application of pyrosequencing to exon 19 deletions. Analysis of exon 21 by pyrosequencing had been succinctly described by Takano et al. [10, 11], but without any data about the specificity, the repeatability or the sensitivity. We first investigated the characteristics of EGFR mutations in the lung cancer cell lines NCI-H1650 and NCI-H1975 and used them as positive controls for the deletion in exon19 and the point mutation in exon 21 respectively. Moreover we used the DNA of these cells mixed with DNA isolated from blood samples from healthy volunteers to evaluate the basic properties of our novel method. We didn’t observe strict linearity

because the two cell lines (NCI-H1650 and NCI-H1975) have respectively 4 and 2.8 EGFR gene copies Fenbendazole [12] but we found good sensitivity. In routine daily practice fixed paraffin-embedded specimens, most often of small size, are the only samples available for both diagnosis and molecular analyses. The DNA is frequently fragmented, which could hamper PCR amplification. However, the PCR conditions described in this study allowed analysis of 96.7% of the paraffin-embedded tissues whatever the type of fixative used or the duration of the fixation. When the samples could be amplified and analyzed, results were concordant (97.4%) with those obtained by conventional BigDye terminator sequencing. The difference in sensitivity between the two methods is illustrated by the 3 samples characterized as mutated only by pyrosequencing.

In this study, we described the expression of these three different proteins associated with multidrug resistance and radiotherapy in chordoma. All the tested markers exhibited some changes in their expression pattern in chordoma compared with normal nucleus pulpous. The most prominent reduction in expression was observed for MDR1 which was very weakly expressed or unexpressed in more than 50% of the chordoma samples studied. To our knowledge, this was the first study on genes associated with resistance to chemotherapy and radiotherapy in spinal

chordoma. The current results showed that MRP1 was expressed in the membranous and intracellular regions; HIF-1α was expressed in the cell cytoplasmic and nuclear learn more QNZ cell line regions, whereas MDR1 was not expressed in the chordoma tissues or CM-319 cell. ABC multidrug transporters also played an important role in the establishment of important biological barriers such as the placenta, the blood-brain barrier, and the blood-testes barrier. Although the over-expression of these transporters was a common phenomenon in chemoresistant

tumor cells, we found that MRP1 and HIF-1α expression was upregulated in most chordoma tissues in comparison to normal tissues. It had been proposed that upregulation of ABC multidrug transporters in cancers may play a role in tumorigenesis by enhancing exposure of tissues to carcinogenic xenobiotics. Interestingly, the expression of MDR1 was not inversely expressed in the chordoma tissues. New data on HIF-1 signaling and the potential for targeted therapies, including combinations of hormonal therapies for cancer and

selective investigational Florfenicol HIF-1α inhibiting small molecules would be discussed. Another mechanism by which hypoxia could increase chemoresistance was to enhance the expression of MDR1 gene via a HIF-1 -dependent regulation [30, 31]. Acknowledgements This work was supported by grants from the National Natural Science Foundation of P. R. China (No. 30873027, No.30973409 and No.30330610) and major issues Foundation of health department in Shaaxi province (No. 2010K13-02-05). The authors thank Dr Lianjia Yang and Ms Yanhua Wen (see more Orthopadepics Department, Tangdu Hospital, the Fourth Military Medical University, Xi’an, P. R. China) for their pathological diagnosis. We thank Ms Yunyan Liu and Ms Qiong Ma (Orthopadepics Department, Tangdu Hospital, the Fourth Military Medical University, Xi’an, P. R. China) for their skillful technical assistance. We are also grateful to Dr Tongtao Yang, Dr Dianzhong Zhang, Dr Yong Zhou and Dr Minghua Zhang (Orthopadepics Department, Tangdu Hospital, the Fourth Military Medical University, Xi’an, P. R. China) for their helpful discussion. References 1. Chugh R, Tawbi H, Lucas DR, Biermann JS, Schuetze SM, Baker LH: Chordoma: the nonsarcoma primary bone tumor. Oncologist 2007, 12: 1344–1350.PubMedCrossRef 2.

pinnipedialis B2/94 and B. ceti B1/94. Acknowledgements Research at the laboratories of the authors is supported by the European Commission (Research Contract QLK2-CT-2002-00918), Ministerio de CFTRinh-172 Ciencia y Tecnología of Spain (Proyecto Proyecto AGL2004-01162/GAN). We thank Maggy Grayon for her contribution on DNA extraction from Brucella strains. References 1. Euzéby JP: List of prokaryotic names with standing in nomenclature. [http://​www.​bacterio.​cict.​fr/​index.​html] 2008. 2. Alton GG, Jones LM, Angus selleck chemicals RD, Verger JM: Techniques for the brucellosis

laboratory Paris, France: INRA 1988. 3. Foster G, Osterman BS, Godfroid J, Jacques I, Cloeckaert A: Brucella ceti sp. nov. and Brucella pinnipedialis sp. nov. for Brucella strains with cetaceans and seals as their preferred hosts. Int J Syst Evol Microbiol 2007, 57: 2688–2693.CrossRefPubMed 4. Scholz HC, Hubalek buy Dasatinib Z, Sedlacek I, Vergnaud G, Tomaso H, Al DS, Melzer F, Kampfer P, Neubauer H, Cloeckaert A, Maquart M, Zygmunt MS, Whatmore AM, Falsen E, Bahn P, Gollner C, Pfeffer M, Huber B, Busse HJ, Nockler K: Brucella microti sp. nov., isolated from the common vole Microtus arvalis . Int J Syst Evol Microbiol 2008, 58: 375–382.CrossRefPubMed 5. Le Fléche P, Jacques I, Grayon M, Al Dahouk S, Bouchon P, Denoeud F, Nockler

K, Neubauer H, Guilloteau LA, Vergnaud G: Evaluation and selection

of tandem repeat loci for a Brucella MLVA typing assay. BMC Microbiol 2006, 6: 9.CrossRefPubMed 6. Marianelli C, Ciuchini F, Tarantino M, Pasquali P, Adone R: Molecular characterization of the rpoB gene in Brucella species: new potential molecular markers for genotyping. Microbes Infect 2006, 8: 860–5.CrossRefPubMed 7. Garcia-Yoldi D, Marín CM, de Miguel MJ, Muñoz PM, Vizmanos JL, López-Goñi I: Multiplex PCR assay for the identification and differentiation of all Brucella species and the vaccine strains Brucella abortus S19 and RB51 and Brucella melitensis Rev1. Clin Chem 2006, 52: 779–781.CrossRefPubMed 8. Foster JT, Okinaka RT, Svensson R, Shaw K, De ADP ribosylation factor BK, Robison RA, Probert WS, Kenefic LJ, Brown WD, Keim P: Real-time PCR assays of Single-Nucleotide Polymorphisms defining the major Brucella clades. J Clin Microbiol 2008, 46: 296–301.CrossRefPubMed 9. Whatmore AM, Perrett LL, MacMillan AP: Characterisation of the genetic diversity of Brucella by multilocus sequencing. BMC Microbiol 2007, 7: 34.CrossRefPubMed 10. Lapaque N, Moriyón I, Moreno E, Gorvel JP: Brucella lipopolysaccharide acts as a virulence factor. Curr Opin Microbiol 2005, 8: 60–66.CrossRefPubMed 11. Perry MB, Bundle DR: Advances in brucellosis research (Edited by: Adams LG). Texas A&M University Press, College Station 1990, 76–88. 12.

This is problematic for the efficient isolation of rAAV from keratinized PT3 cells. However this possibility is worth investigating. Niet aland Nashet al[41,42] identified POLD1 as the central DNA polymerase, which is a leading

strand DNA polymerase, the main mechanism through which AAV DNA replication takes place. The need of PCNA and RFC is also compatible with POLD1 as the main AAV-polymerase as PCNA is the processivity factor for POLD1, and RFC is known to assemble PCNA onto 3′OH primers. RPA was not found essential when using adenovirus-infected cell extracts, in contrast to uninfected cell extracts [41]. In any case these data are also consistent with Christensen and Tattersall [43] who found that these same four proteins (POLD1, Selleck Savolitinib RPA, PCNA, and RFC) were the minimum cellular factors required for MVM DNA rolling-circle replication when using a 3′-dimer junction. However theirin vitroreactions AZD8931 research buy also included MVM NS1 protein and cellular PIF protein. In the latest study by Nashet al[41] it was mentioned that there is one additional protein component (present in P-Cell IA) which was needed but was unidentified. It was further speculated that it was a cellular helicase. To AG14699 approach this question we revisited the PT3vsPT1/NK DNA microarray data to observe if particular DNA helicases or overall helicase activity was higher in PT3.

This approach seems valid as even though we have not done the usual triple-DNA microarray analysis, the real-time quantitative PCR expression data fully confirmed the DNA microarray results across multiple genes. Thus, the Affymetrix microarray data we have in hand appears worthy of study for gleaning suggestive information on the AAV-permissive transcriptome. It was found, as shown in Table2, that the overall helicase activity was not significantly different in PT3 cells, with two helicases being up-regulated and one down-regulated in PT3 versus NK/PT1. While POLD1 was clearly found required for AAVin vitroreplication by Nash et al [41] there is a possibility the DNA

Polymerase alpha might be involved in certain “”alternative”" forms of AAV DNA replication, such as through the use of ROS1 internal origins of replication [45]. Both SV40 and parvovirus H-1 are able to use Polymerase alpha for replication [46,47]. To approach this question we revisited the PT3vsPT1/NK DNA microarray data to observe if DNA polymerase alpha was higher in PT3. The results of the Affymetrix data are shown in Table3, and suggest that DNA polymerase alpha is also significantly up-regulated in PT3 over PT1 and NK. However, the importance of this up-regulation, if any, is not yet determined. One question which arises from this data is how or if the four components are coordinately up-regulated in PT3 cells.

The identity of the bands has been confirmed previously [5]. The glycolipids marked with an asterisk have not been analyzed. Figure 3 Role of bgsB in biofilm formation and bacterial adherence to Caco-2 cells. A Biofilm formation on polystyrene. Microtiter plates were incubated with bacteria for 18 h, non-adherent bacteria removed by washing with PBS, and biofilms stained with crystal violet. Data represent the means ± SEM. *** P < Tukey's multiple

comparison test. B Development of biofilm on polystyrene of E. faecalis 12030 wt, 12030ΔbgsB, and 12030ΔbgsA over time. After incubation periods of ≥ 4 h, E. faecalis 12030 wt elaborated significantly more biofilm than the deletion mutants (P < 0.001, Tukey's multiple comparison test). Bars represent VX-809 ic50 means ± SEM. C Bacterial adherence to Caco-2 cells. Caco-2 cells were incubated at a multiple of infection of 100:1 for 2 h with the respective strain grown to mid-log

click here phase. Data represent the means ± SEM. *** P < 0.001, Dunn's multiple comparison test. Deletion of bgsB leads to a complete loss of glycolipids from the cell membrane and to expression of LTA with increased chain length We hypothesized that, because it is located immediately downstream from bgsA and has high homology to ALmgs in Acholeplasma laidlawii, the gene product of bgsB glycosylates diacylglycerol to yield MGlcDAG. To test this hypothesis, we extracted the total lipids of the cell membrane, separated them by thin layer chromatography (TLC), and stained glycolipids with α-naphthol (Figure 2). As shown previously, inactivation of bgsA resulted in accumulation of OSBPL9 MGlcDAG in the cell membrane (Figure 2). In contrast, no glycolipids were visualized in 12030ΔbgsB extracts, suggesting that bgsB encodes for a glycosyltransferase that glycosylates DAG to form MGlcDAG. MGlcDAG is the substrate of BgsA, which adds a second glucose to yield DGlcDAG (Figure 1). Since BgsA does not accept DAG as a substrate, inactivation of BgsB results in the loss of all glycolipids from the cell membrane (Figure 2). We recently showed

that inactivation of bgsA also affects LTA synthesis, increasing the chain length of the glycerol-phosphate polymer [5]. Inactivation of bgsB has a similar effect on the LTA chain length (Figure 4). To estimate the chain length of the glycerol-phosphate chain by 1H-NMR analysis, we used the fatty acid signals of the molecule as an internal reference and compared the integration values of H1 of glucose and -CH3 of alanine to the -CH3 and -CH2- signals (δ 1.26-1.29, and 0.88) of the fatty acids [5]. The integral ratios yielded higher amounts of glucose and alanine incorporated into the LTA of 12030ΔbgsB and 12030ΔbgsA compared to the wild type, suggesting an increased length of the glycerol-phosphate polymer (Figure 4). These results are Ivacaftor supplier supported by quantification of LTA from butanol extracts by ELISA (Figure 5).