Interestingly, the closest variants to the homB predominant see more allele AI were the rarest variants AV and AVI, all three exclusive of homB gene. The closest variants to the homA predominant allele AII were AIII and

AIV (data not shown). Concerning the most prevalent homB and homA allele types, no geographical predominance of any allele was observed, and no correlation was found between any allelic variant and gastric disease as well (data not shown). In order to test the in vivo expression of homB and homA allelic variants, human sera were tested with a recombinant purified HomB protein, allele type AI [9]. All sera (n = 24) showed an immunoreaction against this protein, suggesting that all homB and homA allelic variants are expressed during infection and are antigenic in humans. However, it should be noted that only one serum could be tested for the rarest allelic variants, AIII, AIV, AV and AVI. Discussion In the present study, the distribution and diversity of two putative H. pylori OMP-coding genes, homB and homA, was evaluated in clinical strains with different geographical origins. Both genes displayed a varied worldwide distribution, with a marked difference between East Asian and Western countries, in accordance with other studies reporting such differences in the frequency of H. pylori virulence factors [16–19]. At least one copy of either homB

or homA genes was found to be present in the genome of the H. pylori strains suggesting that these OMP-coding genes are under selective learn more pressure to be maintained in the bacterium,

as was reported for other H. pylori OMP-coding genes such as babA/babB, sabA and mafosfamide oipA [5–7]. Analysis of homB and homA genes revealed diversity regarding the number of copies and their genomic localization, regardless of the clinical origin of the strain, but with geographical specificity. Both the homB/homA single-copy and the double-copy genotypes were observed in Western strains while the East Asian strains presented the single-copy genotype only, suggesting that, if gene duplication had occurred, it did not seem to be a random event. Variation in copy number of OMP-encoding genes can help the bacterium adapting to a particular host, which is essential to promote a chronic infection [5, 11, 20]. The fact that homB and homA genes display a high level of similarity, especially at the 5′and 3′ ends, suggests that intra or intergenomic recombination events can occur, leading to gene duplication, deletion or homB/homA conversion, as a response to environmental changes. The presence of an intergenic region at the empty locus with high identity with both homB and homA suggests that the gene was lost, leaving short remnant sequences which will enable the gene to be integrated again by genomic recombination, in response to environmental changes, as has been hypothesized for other H.

He proceeded on the reasonable assumption that arithmetic

and its numerical language are the same the universe over. The history of terrestrial mathematics confirms his assumption quite well. Therefore, a preamble of any message should be arithmetical to be easily understood by an intellectual addressee. Needless to say, the natural series as well as examples of arithmetical operations should be presented first of all. Freudenthal selleck inhibitor used for that the so-called “ostensive numerals”, i.e. certain sets of identical radio pulses or “beeps”. He accompanied these numerals with their dyadic notations. Dutil and Dumas (2003) improved Freudenthal’s pattern for a real broadcast. They supplemented those dyadic notations with the decimal ones.

The decimals, among other BKM120 mw things, show the artificial origin of the broadcast itself. Indeed, the place-valued decimal system with zero conception is an indisputable artifact of the mind. Some signs of our knowledge have been broadcast, too. These are the “Egyptian triangle”, the zero sign at the beginning of the natural series, and a structure of DNA. The radio telescope broadcast toward five stars took place in Evpatoria, Ukraine and Roswell, New Mexico, U.S.A. on July 6th 2003. Admittedly, the genetic code—a kingpin of the life information system—holds the key to a mystery of the origin of life. The first thing for a new molecular biology is its strict scrutiny. Therefore, the genetic code itself should be the best place for the preamble, if there were a genetic channel for an intellectual message. Though the following words stagger belief, it seems that such channel exists. The simple and uniform grammar discloses a primordial message incorporated into the genetic code (shCherbak, 2008). Both Freudenthal’s LINCOS pattern and Dutil’s and Dumas’ improvement bear a striking likeness to the contents of this message. First, the genetic code stores internally the

fundamental symbols of arithmetic. They are: the zero, the decimal place-value number system, and numerous summations of nucleons—a kind of “ostensive numerals”—in amino acids. The decimalism Montelukast Sodium shows itself through criterion of divisibility by the prime number 37. There is a set of nucleon sums 000, 111, 222, 333, 444, 555, 666, 777, 888, 999 in the message. The decimal syntax of these sums is reinforced with their exact equilibrations. Another numerical symbol is the “Egyptian triangle”. Such arithmetic asserts the artificial nature of the message and shows a possible mathematical order of genomes. Second, the natural series and zero on its flank align the triplet bases. Such grammar discloses the so-called cooperative symmetry that is the message proper.

Furthermore, based on mean antibiotic resistance across the antibiotics tested, the Brown-Forsythe-Levene test of equality of variances between 7 groups gave a test statistic of F(6,833) = 15.3, p < 0.001. Exposure to ceftazidime and colistin gave a high variance, and the differences between means are statistically significant (F = 61.5, P < 0.001). There was no significant difference in the colony forming unit (CFU) values between the populations exposed to antibiotics in ASM and in populations exposed to ASM alone. ASM appears to generate variation in bacterial numbers among replicates.

Figure 1 buy Tubastatin A Diversification of LESB58 grown in the presence (closed circles) or absence (open circles) of antibiotics. Forty isolates of LESB58 from each culture were characterised using 13 traits (colony morphology, pyocyanin production, hypermutability, auxotrophy, susceptibility to 6 antibiotics and the presence/absence of 3 genomic regions). Therefore, 120 isolates were analysed for each experimental and control group across the 3 replicate populations. Isolates with different traits were identified as being a different haplotype. 3 replicate populations from each of the following treatments were analysed: LB (18 hours), ASM, and ASM with ceftazidime (+ CAZ), ASM with colistin (+CT), ASM with meropenem

(+MEM), ASM with tobramycin (+TOBI), ASM with azithromycin (+AZT). (A) Number of novel haplotypes found within each replicate population. (B) Haplotype diversity found CX-6258 clinical trial within each replicate population, defined as the probability of two randomly picked haplotypes being non-identical. (C) The colony forming units found within each replicate population following culture. P-values represent comparisons with ASM alone. Figure 2 Population structure of LESB58 grown in ASM with and without sub-inhibitory concentrations

of antibiotics. Each population structure of LESB58 was calculated using 13 traits (colony morphology, pyocyanin production, hypermutability, auxotrophy, susceptibility to 6 antibiotics and the presence/absence selleck screening library of 3 genomic regions) for the total 120 isolates by the eBurst algorithm. Each dot (and subsequent number) represents one novel haplotype, with dot size reflecting abundance. The larger the dot size, the more abundant that novel haplotype was in the 120 isolates that we characterised. Haplotypes designated with the number 1 represent isolates with the same characteristics as the P. aeruginosa LESB58 wild-type. The haplotypes representing isolates that had a straw-coloured colony morphology are circled in red; the haplotypes representing isolates that did not over-produce pyocyanin are circled in blue; and the one isolate that was hypermutable is circled in green.

Proteins were transferred to a (polyvinylidene difluoride (PVDF) membrane (Millipore, Bedford,

Massachusetts, USA). The membranes were blocked and epitopes detected with monoclonal antibodies against gp340 (mAb143) [34] or LUM7-2 [35]. Membranes were washed with TBS (gp340) or PBS (MUC7) and incubated with HRP-conjugated anti-mouse (SAB-100, Stressgen, Victoria, Canada) for gp340 or HRP-conjugated anti-rabbit MRT67307 (P0448, DAKO, Glostrup, Denmark) for MUC7 and detected using Super Signal west Dura Extended Duration Substrate (Thermo Scientific, Rockford, IL, USA). Data processing and statistical analyses The power calculation for the parent study was based on body weight as main outcome [36] with a statistical power of 80% and a level of significance of 0.05% (unpublished data, Timby N, Hernell O, Lönnerdal B and Domellöf M). Based on previous investigations [37], IWP-2 the number of infants included in this study was sufficient to detect a difference in bacterial colonization pattern. Data handling and statistical analyses were performed using PASW Statistics

20 (IBM Corporation Route 100, Somers, New York, USA). Anthropometric measures for infants were averaged, and means with 95% CI reported. Differences between means were tested using analysis of variance (ANOVA) followed by a Bonferroni post hoc test. Differences between means for lactobacilli Amino acid detected in saliva and swabs were tested using generalized linear modeling adjusted for delivery method and exposure to probiotic drops at 4 months. L. gasseri detected in swabs was additionally adjusted for amount

of DNA. Categorical data are presented as proportions (%) and differences between groups were tested with a Chi2 test. A p-value <0.05 was considered statistically significant. Multivariate partial least squares analysis (PLS) was performed (SIMCA P+, version 12.0, Umetrics AB, Umeå, Sweden) as previously described [38, 39]. Cross-validation (Q2 values) was performed by a systematic prediction of 1/7th of the data by the remaining 6/7th of the data. The importance of each variable in the model was displayed in a loading scatter plot. R2- and Q2-values give the capacity of the x-variables to explain (R2) and predict (Q2) the outcome. Results Among the 133 infants, the proportions of boys and girls, infants delivered vaginally, mean body weight and length at birth and at 4 months of age (screening age) did not differ significantly between infants fed breast milk, the standard formula or the MFGM-enriched formula (Table 1). This observation was not affected by exclusion of infants given antibiotics or probiotic drops.

Six Syrian hamsters, including three from group A and B (12 wk, 18 wk, and 18 wk, respectively) and three from group C (blank control group), were used as a training group for miRNA microarray analysis. All of the handling measures used with the Syrian hamsters were in accordance with approved guidelines (Guidelines for the Care and Use of Laboratory Animals) established by the Chinese Council on Animal Care. Fabrication of the miRNA microarray The miRNA microarrays were obtained from CapitalBio Corporation (Beijing, China), corresponding to the current release of the Sanger miRNA database (http://​microrna.​sanger.​ac.​uk; August 2007). The individual oligonucleotide probe was SAR302503 chemical structure printed in triplicate on

chemically modified glass slides in a 21 × 21 spot configuration of STA-9090 mw each subarray. The spot diameter was 130 mm, and distance from center to center was 185 mm. A total of 924 mature miRNA sequences were assembled and integrated into our miRNA microarray design. These microarray probes included 677 human miRNAs (including 122 predicted miRNA sequences) [22], 292 rat, and 461 mouse mature miRNAs from the miRNA Registry. All of the oligonucleotide probes

were presented in triplicate in one microarray, and each of the four subarrays contained 16 controls (Zip5, Zip13, Zip15, Zip21, Zip23, Zip25, Y2, Y3, U6, New-U2-R, tRNA-R, hsa-let-7a, hsa-let-7b, hsa-let-7c, 50%DMSO (Dimethyl Sulfoxide), and Hex). The limited sequence length of miRNAs left little consideration for probe design strategy, so all

miRNA probe sequences were designed to be complementary to the full-length mature miRNA. Nucleic acid extraction, labeling, and hybridization Total RNA from each tissue sample was extracted with Trizol reagent (Invitrogen, Carlsbad, USA), and the low-molecular-weight RNA was isolated by a PEG solution precipitation method, according to a previous protocol [23]. We adopted the T4 RNA ligase labeling method according to Thomson’ protocol; that is, 4 μg of low-molecular-weight RNA was labeled with 500 ng of 5′-phosphate-cytidyl-uridyl-cy3-3′ (Dharmacon, Chicago, USA) with 2 units of T4 RNA ligase (NEB, Beijing, China) [24]. The hybridization chamber was laid on a three-phase tiling agitator BioMixerTM II (CapitalBio, click here Beijing, China) to promote microfluidic circulation under the coverslip. The hybridization was performed in a water bath at 42°C overnight. The array was then washed with two consecutive washing solutions (0.2% SDS, 2 × SSC at 42°C for 5 min, and 0.2% SSC for 5 min at room temperature). This procedure was repeated twice for each sample. Microarray imaging and data analysis The miRNA microarray from CapitalBio Corporation was a single-channel fluorescence chip; all oligonucleotide probes were labeled with Cy3 fluorescent dye (green). Fluorescence scanning used a double-channel laser scanner (LuxScan 10 K/A, CapitalBio).

Shrivastava IH, Sansom MS: Simulations of ion permeation through a potassium channel: molecular dynamics of KcsA in a phospholipid bilayer.

Biophys J 2000,78(2):557–570. 10.1016/S0006-3495(00)76616-1CrossRef Selleck LEE011 16. Gunlycke D, Areshkin D, White C: Semiconducting graphene nanostrips with edge disorder. Appl Phys Lett 2007,90(14):142104. 10.1063/1.2718515CrossRef 17. Datta S: Electronic Transport in Mesoscopic Systems. Cambridge: Cambridge University Press; 2002. 18. Amin NA, Mohammad TA, Razali I: Graphene Nanoribbon Field Effect Transistors. Advanced Nanoelectronics 2012, 165–178. http://​www.​crcnetbase.​com/​doi/​abs/​10.​1201/​b13765-6 Competing interests The authors declare that they have no competing interests. Authors’ contributions MJK wrote the manuscript and contributed to the analytical modelling of the presented FET via MATLAB software.

Dr. FKCh and Dr. MTA revised selleck kinase inhibitor the manuscript and coordinated between all the contributors. HKFA, MR, and AH organized the final version of the manuscript. All authors read and approved the final manuscript.”
“Background Coiled carbon materials exhibit a variety of unique characteristics, such as super-elasticity [1], wide band absorption of electromagnetic waves [2], and hydrogen adsorption [3]. In particular, researchers have focused on the preparation [4–9], characterization [10, 11], and growth mechanism [12, 13] of the coiled carbon materials because these helical materials are currently not commercially Progesterone available and they possess great potential applications [14–18]. At present, artificial coiled structures at the mesoscale usually

have simple helical geometries of one-dimensional helical fibers depending on the growth condition such as temperature, flow rate, and carbon source. It was reported that several coiled carbon fibers (CCFs) can be obtained using appropriate catalyst on some substrate or with the help of electric and magnetic field. For example, Chen and Motojima prepared the carbon microcoils by the Ni-catalytic pyrolysis of acetylene containing a small amount of thiophene [19]. Three-dimensional (3D) spring-like carbon nanocoils were obtained in high purity by the catalytic pyrolysis of acetylene at 750°C to 790°C using a Fe-based catalyst, and the nanocoils have a tubular shape of diameter of about 10 to 20 nm [20]. Besides, the carbon nanocoils having coil diameters of 50 to 450 nm can be obtained by applying a magnetic field in the reaction zone or using sputtered thin films of Au and Au/Ni as catalysts [21]. In fact, Ni catalyst plays a significant role in control of the helical structure during the growth of carbon coils [1]. Though several methods of preparing nickel particles, such as hydrothermal reduction technique [22], electrodeposition [23], sol-gel process [24], and microwave irradiation method [25] have been reported, the agglomeration of the particles should be prevented or else this would result to the nonuniformity of the as-prepared Ni particles.

TDF/FTC/COBI/EVG is the most recent LY294002 clinical trial available STR, recommended as preferred in the Department of Health and Human services (DHHS) Guidelines for naïve HIV-infected patients with creatinine clearance (CrCl) >70 mL/min [43, 45, 64]. The integrase inhibitor EVG can be administered OD. The speed of viral suppression observed with TDF/FTC/COBI/EVG is consistent with the potency of HIV integrase inhibitors and robust COBI-boosted EVG exposures [41, 65]. TDF/FTC/COBI/EVG has shown to be non-inferior for safety and efficacy to TDF/FTC/EFV at 48 [51], 96 [52] and 144 weeks [53] in a controlled, randomized trial enrolling 700 HIV-positive cART-naïve subjects (Table 2). At

week 48, 87.6% of the patients receiving TDF/FTC/COBI/EVG had HIV-RNA concentrations <50 copies/mL vs. 84.1% of those receiving TDF/FTC/EFV [57]. HIV-RNA Selleck FHPI concentrations <50 copies/mL were maintained at week 144 in 80% of the TDF/FTC/COBI/EVG arm vs. 75% in the TDF/FTC/EFV arm, testifying for durability [53]. Very few patients in the TDF/FTC/COBI/EVG arm discontinued because of AEs, 4% at week 48 [51] and 5% at week 96 and 6% at week 144 [52, 53]. The most common AEs observed in the TDF/FTC/COBI/EVG arm were nausea and an increase of serum creatinine concentration with a decrease in estimated glomerular

filtration rate (eGFR). COBI is associated with reduced active secretion of creatinine in the renal tubules leading to initial rises in creatinine levels in the first 2–4 weeks [52]. Because of this, only patients with a CrCl >70 mL/min were included in the registrative studies and consequently the use of COBI is currently allowed only in patients with CrCl >70 mL/min. Large pharmacovigilance programs on this enhancer should be considered to look at

its long-term impact on renal function, not limiting data to just eGFR changes. A second, large (715 enrolled patients), non-inferiority double-blind trial compared TDF/FTC/COBI/EVG to atazanavir (ATV)/RTV + FTC/TDF. The primary endpoint was the proportion mafosfamide of patients suppressed at week 48 [54], but secondary endpoint week 96 [55] and 144 [62] data are available. At week 48, 89.5% of the patients receiving TDF/FTC/COBI/EVG had HIV-RNA concentrations <50 copies/mL vs. 86.8% of those receiving ATV/RTV + FTC/TDF [60]. At week 144, the figures were 78% and 75% [56]. As for the previous study, the rate of discontinuation in the TDF/FTC/COBI/EVG arm due to AEs was very low (3.7% at week 48) [54] (Table 1). Furthermore, the TDF/FTC/COBI/EVG-treated patients had statistically lower increases in fasting triglycerides, and a lower percentage of subjects experienced alanine aminotransferase (ALT), aspartate aminotransferase (AST) or bilirubin elevations when compared with ATV/RTV + TDF/FTC-treated patients. As for resistances, in the 102 study [51], 2% of patients in the TDF/FTC/COBI/EVG arm failed with resistance inducing mutations, usually to both NRTIs and EVG. The result was comparable to that observed in the TDF/FTC/EFV arm.

Small molecule tyrosine kinase inhibitors and monoclonal antibodies are among the most common EGFR targeting agents and have been used clinically for

treating various malignancies [26]. Recently, it was reported that mutations in the tyrosine kinase domain of EGFR gene can predict the response to tyrosine kinase inhibitors [27]. And if alleles with EGFR mutations are amplified, the response to tyrosine kinase inhibitors may differ relative to mutant alleles without gene amplification [28]. Thus, EGFR mutations enable the identification of the glioma subgroup that is likely to be addicted to EGFRs. Losses of chromosomes 1p and 19q are deemed correlated with the diagnosis of oligodendroglioma, higher PCV chemosensitivity and favorable prognosis [29]. The average rates of 1p deletion and 1p/19q codeletion were

respectively 65.4 and 63.3% in oligodendrogliomas, Copanlisib concentration 28.7 and 21.6% in oligoastrocytomas, 13.2 and 7.5% in astrocytomas, 11.6 and 2.9% in glioblastomas [30]. Established indicators of the favorable outcome of oligodendroglial tumors include LOH on chromosomes 1p and 19q, which may indicate a loss of function of as yet unknown tumor-suppressor genes located in those regions [31]. LOH of 1p EPZ5676 mw in the heterogeneous population of malignant gliomas may be one of the vital factors besides MGMT promoter methylation that predict better outcome in patients treated with TMZ [32]. Mutations in IDH1/2 are a common feature of a major subset of primary human brain tumors [33]. Recent studies reported that mutations usually affected amino acid 132 of IDH1 in more than 70% of grade II-III gliomas and secondary glioblastomas. Tumors without mutations in IDH1 often had mutations affecting the analogous amino acid (R172) of the IDH2 gene. Tumors with IDH1 or IDH2 mutations had distinctive genetic and clinical characteristics, and patients with such tumors had a better outcome than those with wild-type IDH genes Hydroxychloroquine [34, 35].

IDH1 mutation contributes to tumorigenesis partly through induction of the HIF-1 pathway [36]. And it has been recently reported that tumor-derived IDH1 and IDH2 mutations reduced α-KG and accumulated a α-KG antagonist, 2-hydroxyglutarate (2-HG), leading to genome-wide histone and DNA methylation alterations [37]. 2-HG accumulation caused by IDH mutation was also reported to be involved in the formation of malignant gliomas [38]. A recent study has demonstrated that IDH mutation was correlated with a higher rate of response to temozolomide and appeared to be a significant marker of positive prognosis in low-grade gliomas [39]. Taken together, mutations in IDH genes seem to arise from a common glial precursor and play an important role in the formation of specific glioma subtype in which IDH1/2 mutation functions as oncogene addiction. MicroRNAs (miRNAs) belong to a recently discovered class of small non-coding RNA molecules that regulate the expression of multiple target genes.

In our study, two members of the MMP family, MMP-14 and MMP-28, had increased expression resulting from HIF-1α overexpression in the in vitro microarray experiment and in the CAM experiments. The increased Lazertinib price expression of MMP-14 has been identified as a negative predictor of survival in SCLC [41], and the targeted drug inhibiting MMP-14 expression, marimastat [42], has been used in clinical studies. MMP-28 is expressed at low levels in normal lung tissue, but the expression of MMP-28 is highly increased after cancer formation [43]. MMP-28 induces epithelial-mesenchymal transitions (EMT), which yield tumor cells with collagen-invasive properties allowing the invasion of collagen matrices

[44]. The upregulation of MMP-28 by HIF-1α enhances this ability. The expression level of angiogenic factors is the gold standard to measure the angiogenic potential of tumors, and the inhibition of the expression of angiogenic factors is the primary treatment for SCLC. Angiogenic factors that are significantly regulated by HIF-1α in a hypoxic selleck kinase inhibitor microenvironment are also therapeutic target points [45]. In addition to VEGF, FGF-2 [46], ANG-2 [47], HIF-2α [48], and PDGFC are also involved in tumor angiogenesis. In this study, three inflammatory factors, IL-6, TNFAIP6, and IL1R1, were upregulated by HIF-1α. These inflammatory factors actively responded during the process of inflammatory

angiogenesis. TNFAIP6 is the stimulating factor for TNF-α [49], and IL-1R1 is the receptor for IL-1 [50]. IL-6 and VEGF-A have synergistic effects in stimulating the proliferation and invasiveness of tumors by promoting angiogenesis [51]. Our results indicate that HIF-1α may enhance the inflammatory reaction or stimulate

the secretion of coherent inflammatory factors to promote the angiogenesis of SCLC, which highlights the importance of anti-inflammation for the treatment of SCLC as some scholars have suggested [52]. In addition, the TNC, FN1, and HMOX1 cytokines were screen out by microarray analysis. TNC is an extracellular matrix protein with angiogenesis-promoting activities, Amobarbital and it has specific functions in vessel formation [53]. FN1 has been shown to be an angiogenic cytokine involved in angiogenesis during several pathological processes, such as psoriasis, diabetic retinopathy, and cancer [54]. The overexpression of HMOX1 has been observed in liver cancer [55], pancreatic cancer [56], and melanomas [57]. Targeting these cytokines for gene therapy of SCLC in the future requires their verification in clinical trials. Conclusions Overall, our results suggest that HIF-1α significantly promotes the growth and angiogenesis of NCI-H446 cells by upregulating the expression of angiogenic genes. Moreover, our use of the chick CAM as an in vivo experimental model further confirms the expression of these genes induced by HIF-1α.

PFGE typing was undertaken at the Moredun Research Institute, Scotland, UK and VISAVET, Madrid, Spain. IS900-RFLP typing check details was carried out at the Veterinary Research Institute in Brno, Czech Republic and VISAVET. Published standardized typing procedures were used as described in Materials and Methods. The only difference

in procedures between laboratories was that at VISAVET the IS900-RFLP analysis was performed using the agarose plugs prepared for PFGE to avoid having to perform two separate DNA preparations for the different typing techniques. The correct profiles were reported by all laboratories for the duplicate isolates included to check reproducibility. All typing techniques correctly reported that the Mycobacterium phlei (M. phlei), Mycobacterium bovis BCG (M. bovis BCG) and IS901 positive M. avium were not Map. One field isolate, EU112 was found to be IS901 positive M. avium (it GSK2118436 cost is not known if the isolate is M. avium subsp. avium or M. avium subsp. silvaticum) and not Map as was originally suspected. Another isolate, EU169 was

found to be a mixed culture. Isolates one to 50 were typed at Institut für Mikrobiologie Stiftung Tierärztliche Hochschule Hannover, Hannover, Germany using the Type I/Type II PCR as described by Dohmann et al. [17]. EU25 and EU30 were identified as Type I and all other field isolates as Type II. These results correlated with the strain type as determined Atazanavir by PFGE. This PCR [17] cannot

discriminate between Type I and Type III and as strain types could be discerned from the PFGE profiles, it was not considered necessary to determine the strain type of the remaining isolates by PCR. It was not possible to type all of the isolates with all typing methods as some laboratories had difficulties in subculturing some isolates to prepare sufficient cells for analyses. A total of 123 Map isolates were typed by IS900-RFLP, PFGE and MIRU-VNTR. IS900-RFLP typing IS900-RFLP typing data were obtained for 147 Map isolates (Table 1 and see supplementary dataset in Additional file 1). It was not possible to obtain PstI profiles for 55 isolates or clear BstEII profiles for five isolates. There was a problem using agarose plug DNA for IS900-RFLP typing with PstI as the enzyme would not cleave in the presence of agarose. Extraction of the DNA from the agarose and repeat PstI digestion was not attempted. As expected, profiles were not obtained for the negative control strains M. bovis BCG, M. phlei and IS901 positive M. avium. A total of six PstI profiles were found among 93 isolates: B (n = 88); G (n = 1); I (n = 1); K (n = 1); R (n = 1); and U (n = 1). Seventeen BstEII profiles were detected among 142 isolates: C1 (n = 71); C17 (n = 49); C5 (n = 5); C9 (n = 3); C16 (n = 2) and single isolates with C10, C18, C22, C27, C29, C35, C36, C38, C39, S4, I4 and I5.