J Antimicrob Chemother 2006; 58 (5): 960–5.PubMedCrossRef 73. Lister PD. Pharmacodynamics of levofloxacin against characterized ciprofloxacin-resistant Streptococcus pneumoniae.

Postgrad Med 2008; 120 (3 Suppl. 1): 46–52.PubMedCrossRef 74. Brinker A. Telithromycin-associated hepatotoxicity [online]. Available from www.​fda.​gov/​ohrms/​dockets/​AC/​06/​slides/​2006-4266s1-01-07-FDA-Brinker.​ppt learn more [Accessed 2012 Jan 28].”
“Introduction Blood pressure (BP) control rates are improving but are still far from adequate. The latest report stated that BP control has improved considerably from 25% to 50% at present.[1] Although these control rates may be true for the recommended BP goals of <140/90 mmHg for uncomplicated hypertension, the control rates for the more aggressive goal of <130/80 mmHg for persons with diabetes mellitus, chronic renal disease, or coronary heart disease (CHD) are lower.[2–5] selleck chemicals llc Most studies show that in order to reach these goals, the majority of patients will require two or more

antihypertensive drugs.[6–10] Calcium-channel blockers (CCBs) and angiotensin-converting enzyme (ACE) inhibitors are still recommended for first-line therapy for hypertension,[2,3] but given alone, do not produce BP reductions to currently recommended BP goals, and in most patients with stage 2 hypertension, a combination of two drugs from different classes is recommended.[2–4] The combination of a CCB with an ACE inhibitor is particularly attractive for patients with diabetes or hyperlipidemia because both drugs are metabolically

neutral. In addition, the combination of an ACE inhibitor with amlodipine, a dihydropyridine CCB, will increase the latter’s antihypertensive VX-689 mouse effect[11–14] and ameliorate the incidence and magnitude of pedal edema.[11,12] The currently available fixed-dose combination of amlodipine/benazepril 5/10 and 10/20 mg/day has been effective in reducing BP, but more aggressive treatment of hypertension with higher-dose combinations may be necessary to bring BP to goal, especially in populations like Black patients, who are resistant to treatment.[13] Several clinical trials have shown that the combination of ACE inhibitors or angiotensin-receptor blockers (ARBs) with a CCB is synergistic and provides Ribonucleotide reductase greater reductions of BP in a variety of hypertensive populations, and the vasodilatory edema seen with the dihydropyridine CCBs is usually decreased with their combination.[11,12,15–18] In this report, we present the effectiveness and safety of a high-dose combination of benazepril with amlodipine in Black and White hypertensive patients compared with high-dose monotherapy with benazepril hydrochloride 40 mg/day or amlodipine besylate 10 mg/day. Subjects and Methods Study H2303 consisted of 291 completed subjects and study H2304 consisted of 763 completed subjects. All subjects were well matched for age and sex and other clinical parameters.

We have also found that statins induce click here apoptosis by activation of caspase-3 through learn more inhibition of GGPP biosynthesis. It has been reported that statins inhibit prenylation of small G proteins by suppressing the production of GGPP [4, 8]. Lovastatin is known to inhibit the mevalonic acid and MAPK pathways, thereby inducing apoptosis [9, 10]. It has been reported that the mechanism of action is inhibition of GGPP biosynthesis [10, 11]. These findings suggest that statins induce apoptosis by activation of caspase-3 through suppression

of GGPP biosynthesis. GGPP is an important membrane-anchoring molecule of Ras protein. A shortage of GGPP facilitates dissociation of Ras from the inner surface of the membrane, and decreases the Ras-mediated growth signal, thereby inhibiting cellular proliferation [12, 13]. Our results clearly demonstrate that statins induce a decrease in ERK1/2 and Akt activation of Ras downstream, Palbociclib concentration but the activation of JNK1/2 was not altered. We previously reported that mevastatin induces a decrease in phosphorylated ERK [3]. We also demonstrated that fluvastatin and simvastatin decrease the activation of ERK1/2 Akt [4]. These findings are in agreement with the results of the present study and indicate that

statins induce apoptosis via suppression of Ras/ERK and Ras/Akt pathways in our experimental model (Figure 5). Figure 5 Schematic representation of interacellular effects of statins in C6 glioma cells. As described above, statins are known to affect the

functions of Ras by inhibiting prenylation through the inhibition of GGPP synthesis; this enables localization of Ras at the plasma membrane [14, 15]. Ras is involved in the activation of the MEK/ERK and PI3K/Akt pathways [14, 16], suggesting the mechanism of action of statins. The treatment of C6 glioma cells with 5 μM mevastatin, 5 μM fluvastatin or 10 μM simvastatin for 72 h in vitro inhibited GGPP synthesis. very We also found that the treatment of C6 glioma cells with 2.5 μM mevastatin, 1 μM fluvastatin or 5 μM simvastatin for 72 h inhibited cell proliferation. The peak plasma concentrations of fluvastatin or simvastatin achieved with standard doses were ≤ 1 μM or 2.7 μM, respectively [17, 18]. It has been reported that peak plasma concentration of fluvastatin achieved with high dose were ≤ 2 μM [19]. These findings indicate that 2 μM and 2.5 μM of fluvastatin and simvastatin, respectively, are within the peak plasma values of fluvastatin or simvastatin that are likely to be achieved in vivo. In addition, we found that 2.5 μM fluvastatin induced the apoptosis. Therefore, fluvastatin may be potentially useful as anti-cancer agents in the treatment of glioblastoma. Conclusion In conclusion, these results provide evidence of the specific molecular pathways via which statins induce apoptosis by increasing the activation of caspase-3 through inhibition of Ras/ERK and Ras/Akt pathways.

5% of the DNA was mutated. Table 3 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). selleck compound 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 selleck 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 selleck chemicals llc strict linearity

because the two cell lines (NCI-H1650 and NCI-H1975) have respectively 4 and 2.8 EGFR gene copies Edoxaban [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.

The pellet was washed twice in cold 0.1% Triton X-100 PBS and incubated at room temperature for 30 minutes with 300 μL DNA dye (containing 100 μg/mL propidium iodide and 20 U/mL RNase; Sigma Corporation). Flow cytometry analysis (BECKMAN-COULTER Co.,

USA) was performed. The cells were collected for the calculation of DNA amount for cell cycling analysis using a MULTYCYCLE software (PHEONIX, Co. USA). The extent of apoptosis was analyzed and quantified using WinMDI version 2.9 (Scripps Research Institute, La Jolla, CA, USA). Differential expression of LY3023414 solubility dmso microRNAs Preparation of total RNA sample A549 cells were cultured in 6-well plates (1.5 × 105 cells per well) and treated for 72 h with 10 μmol/L bostrycin for the bostrycin group or with complete medium for the control group. C646 clinical trial The cells were lysed in 1.5 mL of Trizol reagent and total RNA was prepared according Thiazovivin to the manufacturer’s instructions. Microarray Microarray analysis was performed using a service provider (LC Sciences, USA). The assay used 2-5 μg total RNA, which was size-fractionated using a YM-100 Microcon centrifugal filter (SIGMA). The small RNAs (<300 nucleotides) isolated were 3' extended using poly(A) polymerase. An oligonucleotide tag was then ligated to the poly(A) tail for fluorescent dye staining. Two different tags were used for the two RNA samples in dual-sample experiments.

Hybridizations were performed overnight on a μParaflo microfluidic chip using a

microcirculation pump (Atactic Technologies, Adenosine triphosphate Houston, TX, USA). Each detection probe on the microfluidic chip consisted of a chemically modified nucleotide-coding segment complementary to a target microRNA (miRBase; http://​microrna.​sanger.​ac.​uk/​sequences/​) or other RNA (control or customer-defined sequences). The probe also contained a spacer segment of polyethylene glycol to separate the coding segment from the substrate. The detection probes were made by in situ synthesis using PGR (photogenerated reagent chemistry). The hybridization melting temperatures were balanced by chemical modifications of the detection probes. Hybridization was done in 100 μL 6 × saline-sodium phosphate-EDTA buffer (0.90 M NaCl, 60 mMNa2HPO4, and 6 mM EDTA, pH 6.8) containing 25% formamide at 34°C and fluorescence labeling with tag-specific Cy3 and Cy5 dyes was used for detection. Hybridization images were collected using a laser scanner (GenePix 4000B, Molecular Device) and digitized using Array-Pro image analysis software (Media Cybernetics). Data were analyzed by first subtracting the background and then normalizing the signals using a LOWESS filter (locally weighted regression). For two-color experiments, the ratio of the two sets of detected signals (log 2 transformed; balanced) and P values of the t test were calculated. Differentially detected signals were those with P < 0.01.

The color change implies nucleation and subsequent growth of nanocrystals due to the decomposition of as-formed metal thiolates. To investigate the growth process of CGS nanoplates, the selleck inhibitor samples collected at different reaction LCZ696 cell line times were characterized by SEM, TEM and XRD, as shown in Figure 4. From Figure 4a (a1), it was surprisingly found that the sample collected at the early reaction stage was not CGS but binary copper sulfides (Additional file 1: Figure S2). As the

reaction further proceeded, the samples mainly contain CGS along with the decrease of binary copper sulfides (Figure 4a (a2 to a6)). When the reaction was performed for 40 min, the product (Figure 1) was pure CGS nanoplates with a hardly detectable binary copper sulfide phase. Hence, in the growth process of CGS nanoplates, copper sulfides firstly formed, and then the as-formed copper sulfides were gradually phase-transformed to CGS nanoplates with Erastin ic50 proceeding of the reaction. The formation of copper sulfides in the early reaction stage maybe results from the difference of the reaction reactivity of two cationic precursors. From Figure 4b,c,d,e,f,g, it was clearly observed that all these intermediate samples were hexagonal nanoplates and the diameter of the nanoplates became uneven with the prolonged reaction, which may be due to the

Ostwald ripening growth process. Figure 4 XRD patterns (a) and SEM images (b, c, d, e, f, g) of samples collected at different reaction times. (a1, b) 220°C, 0 min; (a2, c) 250°C, 0 min; (a3, d) 270°C, 0 min; (a4, e) 270°C, 10 min; (a5, f) 270°C, 20 min; (a6, g) 270°C, 30 min. The inset in b is the corresponding TEM image. Finally, the ultraviolet–visible absorption spectrum of as-synthesized CGS nanoplates has been measured at room temperature, as shown in Figure 5. A broad shoulder in the absorption spectrum can be observed at approximately 490 nm. According to the absorption spectrum, the optical bandgap of CGS can

be estimated by using the equation of (αhv) n  = B(hν - E g), where α is the absorption coefficient, hν is the photo energy, Resveratrol B is a constant, E g is optical bandgap, and n is either 1/2 for an indirect transition or 2 for a direct transition. As a direct bandgap semiconductor, the optical bandgap of CGS was estimated by extrapolating the linear region of a plot of (αhv)2 versus hv (shown in the inset of Figure 5). The estimated optical bandgap of as-synthesized CGS nanoplates is 2.24 eV. The bandgap is smaller than the literature value for wurtzite or zincblende CGS [20], which may be caused by the copper-rich composition of the as-synthesized nanoplates. Figure 5 Absorption spectrum of as-synthesized CuGaS 2 nanoplates. The bandgap is determined from the plot of (αhv)2 vs. photon energy (shown in the inset).

Trupp S, Alberti M, Carofiglio T, Lubian E, Lehmann H, Heuermann R, Yacoub-George E, Bock K, Mohr GJ: Development of pH-sensitive indicator dyes for the preparation Everolimus of micro-patterned optical sensor layers. Sensors Actuators B-Chem 2010,

150:206–210.CrossRef 5. Mohr GJ, Muller H, Bussemer B, Stark A, Carofiglio T, Trupp S, Heuermann R, Henkel T, Escudero D, Gonzalez L: Design of acidochromic dyes for facile preparation of pH sensor layers. Anal Bioanal Chem 2008, 392:1411–1418.CrossRef 6. Sridhar V, Takahata K: A hydrogel-based passive wireless sensor using a flex-circuit inductive transducer. Sensors Actuators a-Phys 2009, 155:58–65.CrossRef 7. Sciacca B, Secret E, Pace S, Gonzalez P, Geobaldo F, Quignarda F: F. C: Chitosan-functionalized porous

silicon optical transducer for the detection of carboxylic acid-containing drugs in water. J Mater Chem 2011, 21:2294–2302.CrossRef 8. Wu J, Sailor MJ: Chitosan hydrogel-capped porous SiO2 as a pH responsive nano-valve for triggered release of insulin. Adv Funct Mater 2009, 19:733–741.CrossRef 9. Perelman LA, Moore T, Singelyn J, Sailor MJ, Segal E: Preparation and characterization of a pH- and thermally responsive poly(N-isopropylacrylamide-co-acrylic acid)/porous SiO2 hybrid. Adv Funct Mater 2010, 20:826–833.CrossRef 10. Low SP, Voelcker NH, Canham LT, Williams KA: The biocompatibility of porous silicon in tissues of the eye. Biomaterials 2009, 30:2873–2880.CrossRef 11. Jane A, Dronov R, Hodges A: N.H V: Porous silicon biosensors on the advance. Trends Biotechnol 2009, 27:230.CrossRef 12. Sciacca B, Frascella selleck inhibitor F, Venturello A, Rivolo P, Descrovi E,

Giorgis F, Geobaldo F: Doubly resonant porous silicon microcavities for enhanced detection of fluorescent organic molecules. Sensors Actuators B-Chem 2009, 137:467–470.CrossRef 13. Orosco MMPC, Miskelly GM, Sailor MJ: Protein-coated porous silicon photonic crystals for amplified optical detection of protease activity. Adv Mater 2006, 18:1393–1396.CrossRef 14. Fauchet PM: Porous silicon: photoluminescence and electroluminescent devices. Semiconductors Semimetals 1998, 49:205–252.CrossRef 15. Szili EJ, Jane A, Low SP, Sweetman M, Macardle P, Kumar S, Smart RSC, Voelcker NH: Interferometric porous silicon transducers using Dehydratase an enzymatically amplified optical signal. Sensors Actuators B-Chem 2011, 160:341–348.CrossRef 16. Pace S, Vasani RB, Cunin F, Voelcker NH: Study of the optical properties of a thermoresponsive Epigenetics inhibitor Polymer grafted onto porous silicon scaffolds. New J Chem 2013, 37:228–235.CrossRef 17. Martin TP, Gleason KK: Combinatorial initiated CVD for polymeric thin films. Chem Vap Depos 2006, 12:685–691.CrossRef 18. Suchao-in N, Chirachanchai S, Perrier S: pH- and thermo-multi-responsive fluorescent micelles from block copolymers via reversible addition fragmentation chain transfer (RAFT) polymerization. Polymer 2009, 50:4151–4158.CrossRef 19.

Figure 4 msmeg0615 (pr1) promoter activity.

β-galactosidase activity of cultures grown in Sauton medium in the presence of varying divalent metal ions. The values, expressed as nanomoles of o-nitrophenol-β-D-galactopyranoside Ruxolitinib converted to o-nitrophenol min-1 mg-1 of protein, represent the average and the standard deviation of three independent clones. * indicates that values are significantly different from the control value (p < 0.01). 5'-RACE and transcriptional analysis of pr2 Cluster 3 gene organization seems to exclude the presence of internal promoter regions with one exception; the distance between the ppe (rv0286, msmeg0619) and esxG (rv0287, msmeg0620) coding regions suggested the presence of an internal putative promoter upstream of M. tuberculosis esxG and the corresponding homologous msmeg0620 gene (Figures 1, 2B). The short rv0287-rv0288 and msmeg0620-msmeg0621 intergenic regions were not analyzed, as the two genes had previously been reported to be cotranscribed [18]. To determine SAHA HDAC nmr whether the putative pr2 promoter was present, we amplified the rv0286-rv0287 and the msmeg0619-msmeg0620 intergenic regions (Figure 2B) and cloned them into pMYT131. The

recombinant plasmids were MK-0518 clinical trial transformed into M. smegmatis, and β-galactosidase activity was measured. As shown in Figure 5, the data suggest the presence of an alternative promoter just upstream of the esx genes, as enzymatic activity, particularly for the msmeg0619-msmeg0620 intergenic region was significantly higher than that measured in the control culture (M. smegmatis transformed with the empty vector). The data regarding M. tuberculosis are less clear, since detectable promoter activity was low. Figure 5 msmeg0620 (pr2 MS) and rv0287 (pr2 MT) promoter activity. β-galactosidase activity of msmeg0620 and rv0287 (pr2) in M. smegmatis cultures grown in 7H9 medium at mid-log phase.

The value find more represents the average and the standard deviation of three independent clones. * indicates that values are significantly different from the control value (p < 0.01). To better define promoter sequences, we performed 5′ RACE experiment. The transcriptional start site, indicated with an arrow in Figure 2B, mapped at -34 upstream of the msmeg0620 translational start codon. Although no SigA promoter consensus sequence was observed in the upstream region, we could found hypothetical -10 and -35 sequences that resembled those reported as to be possibly recognizable by M. tuberculosis SigH factor [19]. We did not identify any pr2 promoter sequence in M. tuberculosis, as the 5′ RACE experiments were unsuccessful. Quantitative PCR on msmeg0615 and msmeg0620 genes and their homologs in M. tuberculosis M. smegmatis mc2155 was grown at different growth phases and in different stress conditions; RNA was extracted, retrotranscribed and used in relative quantitative PCR (qPCR) experiments.

stephensi (Panel A) or An. gambiae (Panel B) females infected with P. yoelii. Live parasites are detected with green fluorescence (left panels), and those melanized are in DIC images (right panels). Panel C, Number of live (green dots) or melanized (black dots) parasites present on individual midguts 6 days PI. The median number of oocysts is indicated by the Protein Tyrosine Kinase inhibitor horizontal line.

Distributions are compared using the Kolmogorov-Smirnov test; n = number of mosquitoes; P values lower than 0.05 are consider to be significantly different. Panel D, The number of live (green dots) and melanized (black dots) P. yoelii parasites on individual An. gambiae midguts is shown connected by a line. In most mosquitoes, either all parasites are alive or all are melanized. There are very few midguts in which both live and melanized parasites

Selleck YM155 are observed. Table 2 An. gambiae (G3) and An. stephensi (Nijmegen Sda500) infections with P. yoelii. Mosquito species Saracatinib clinical trial Prevalence of infection Median live oocyst number Oocyst range % of midguts with melanized parasites % of midguts with live and melanized parasites An. gambiae n = 59 52% 1 0–65 59% 10% An. stephensi n = 47 100% 51 2–302 0% 0% Effect of silencing An. stephensi orthologs on P. yoelii infection Six genes whose phenotypes differ when An. gambiae is infected with P. berghei or P. falciparum were examined. An. stephensi orthologs of OXR1, Hsc-3, GSTT1, and GSTT2, as well as two other genes previously reported in the literature (LRIM1 and CTL4), Fossariinae were silenced, and the effect on P. yoelii infection was evaluated. Five of the six genes

tested had similar effects in the An. gambiae-P. falciparum and the An. stephensi-P. yoelii systems (Table 1). Silencing OXR1, LRIM1, CTL4, or GSTT1 had no effect, while GSTT2 and Hsc-3 silencing enhanced P. yoelii infection in An. stephensi (Figure 4 and Table 1). Hsc-3 was the only gene that gave a different phenotype between An. gambiae-P. falciparum and An. stephensi-P. yoelii. Conversely, this was also the only gene that had a similar phenotype in An. gambiae infected with P. berghei and in P. yoelii-infected An. stephensi. The expression of heat shock proteins is temperature dependent; thus the differences in the effect of Hsc-3 silencing in mosquitoes infected with different Plasmodium species could be due to physiologic differences resulting from the temperature at which infected mosquitoes are kept. For example, Hsc-3 silencing decreases P. falciparum infection (26°C) in An. gambiae but results in a significant but mild increase in P. yoelii infection (24°C) in An. stephensi and a strong enhancement of P. berghei infection (21°C) in An. gambiae. Interestingly, a decrease in parasite number is also observed in the Drosophila line in which a P-element has been inserted close to the Hsc-3 gene. In the fly system, in vitro cultured P.

Conversely, over half the isolates analyzed have HST 7 (54%), but by PFGE analysis, these are represented by 18 different PFGE patterns, the most frequent being JF6X01.0022 (48%). Collectively, this data highlights the strengths and weakness of each subtyping method. S. Typhimurium analysis and sequence

type distribution CRISPR-MVLST analysis of 86 S. Typhimurium clinical isolates (representing 45 unique PFGE patterns) resulted in the identification of 37 unique and novel S. Typhimurium Sequence Types (TSTs), TST9 – TST41, and TST56 – TST58 (Table 4). This included 17 CRISPR1, 23 CRISPR2, 4 fimH and 5 sseL alleles (Table 2). Of these, the majority of CRISPR1 alleles were new (15/17 alleles) and all CRISPR2 alleles were new (23/23),

as compared to our previous studies [33]. As with S. Heidelberg, learn more the majority of unique sequence types were defined by polymorphisms in either or both of the CRISPR Selleck GSK126 loci (Figure 2c). Discriminatory power of CRISPR-MVLST and PFGE in S. Typhimurium isolates The discriminatory power of CRISPR-MVLST among the S. Typhimurium isolates was 0.9415 (Figure 4a). This means that there would be a 94% probability that two unrelated isolates could be separated using the CRISPR-MVLST scheme. Similarly, for PFGE, the discriminatory power among these isolates is 0.9486 (Figure 4b). These values suggest that either method can provide sufficient discrimination between outbreak and non-outbreak selleck S. Typhimurium

strains. Figure 4 Frequency of S. Typhimurium subtype prevalence generated by CRISPR-MVLST and PFGE. Pie charts showing the number of distinct find more subtypes defined by a) CRISPR-MVLST and b) PFGE among 86 S. Typhimurium isolates. The most frequent TSTs or PFGE patterns observed are indicated. .0003 and .0146 represent PFGE profiles JPXX01.0003 and JPXX01.0146, respectively. The number of distinct subtypes defined by each method is listed in parenthesis and the discriminatory power (D) is listed below. Correlation between different TSTs and PFGE patterns We next wanted to investigate whether any correlation existed between TSTs and PFGE patterns. To accomplish this, we first determined the relationship among different TSTs. BURST analysis of all 37 TSTs generated four groups (Figure 5a). Of these, Groups 1–3 contain 6 – 15 TSTs. Group 4 consists of only two TSTs and BURST was unable to assign a core TST. There was also a collection of five singletons that BURST did not assign to a group. For Groups 1–3, each group comprises a core TST surrounded by TSTs that differ from the core by one allele. The number of rings in the group demonstrates the number of allele differences from the core. For example, in Group 1 TSTs 9, 37, 32, 20, and 14 each differ by one allele at one locus from the core TST, TST 13. For group 3, TST 10 is the core TST and TSTs 15, 31, 36, 29, 23 and 16 each differ from TST 10 at one locus.

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