The remaining high quality sequences were taxonomically identified using the Classifier tool at a 60% confidence level. The classifier

output was then used for analysis of similarities and difference between herds (Additional files 1, 2, 3, 4, 5). For analysis of the data at the genus level, all genera with fewer than 5 representatives were dropped from the analysis. To identify members of the family Pasteurellaceae and genus Streptococcus Selleck JQ1 to the lowest possible phylogenetic level, we obtained all the 138 near full-length type sequences from family Pasteurellaceae and genus Streptococcus from RDP release 10.22 (August 2010). We also added sequence AF486274 (“”Actinobacillus porcitonsillarum”"). selleck compound These 139 sequences were aligned by the Infernal aligner [16] trained by RDP [17].

The final reference set contained the region corresponding to the 454 FLX amplicon (E. coli position 578 to 784) sliced from the alignment. To determine the nearest neighbor, the 454 FLX sequences passing the RDP Pyro initial filtering were aligned by the Infernal aligner and the distance between each FLX sequence and reference sequences was calculated. The reference sequence with the closest distance was reported. In case of tie, all the reference sequences were reported. Statistical analysis For the statistical analyses of sequences, we used a 0.03% cutoff value for clustering. This is consistent with previous analyses

of 454 data [18] as well as the historical value frequently used over the past 15 years [19, 20]. Similarly we used this cutoff in evaluating members of family Pasteurellaceae and genus Streptococcus. For comparative statistical analyses, aligned sequences were clustered using the RDP Complete Linkage Clustering Tool and the resulting cluster files were used to calculate Jaccard and Sørensen indices [17]. Celastrol For comparative statistical analyses, aligned sequences were clustered using the RDP Complete Linkage Clustering Tool and the resulting cluster files were used to calculate Jaccard and Sørensen indices [17]. Cluster files were also reformatted with the EstimateS Formatter Tool through the RDP website. Principle component analysis followed by centroid calculations with a 95% confidence limit were performed in R (version 2.10; http://​www.​r-project.​org/​) with Vegan package (http://​vegan.​r-forge.​r-project.​org) using the EstimateS formatted files. Chao 1 was calculated using the cluster files derived from each sample and from merged samples for herds using the RDP Pyrosequencing Pipeline. Simpson’s Diversity index was calculated with MOTHUR [21]. Results Community DNA was isolated from whole tonsil tissue (Pigs A-M) or tonsil brushings (Pigs J-M) as described in Methods. Tonsil tissue samples were collected in spring 2007 from two different herds, and again in spring 2009 from Herd 1.

Oppositely, the wounds were still

widely open at 24 hours after exposure to PTL at indicated concentrations. The results indicated that PTL treatment could inhibit migration of pancreatic cancer cell. Figure 3 PTL suppressed BxPC-3 migration. The wound gap of cells was scratched by a micropipette tip. Cells were incubated in the presence of PTL. 24 hours BMN-673 later the wound gap of BxPC-3 in the control group was nearly closed. On the contrary, after exposure to PTL at 7.5 μM, the speed of wound closure was much slower and the wound was still widely open at twenty-four hours. PTL inhibited BxPC-3 cell invasion The effect of PTL on BxPC-3 cell invasion was detected by a reconsitituted Matrigel membrane. The number of cells that passed through the filter and into the lower chamber was counted and compared. As a result, PTL at different concentrations obviously inhibited invasive ability of pancreatic cancer cell. The cell numbers of 7.5 μM and 15 μM PTL groups were (94 ± 7)/HPF and (58 ± 8)/HPF respectively, which were less than (146 ± 10)/HPF of control group (P < 0.05) (Fig. 4). Figure

4 PTL inhibited BxPC-3 cells invasion. Cells were fixed, stained and counted at 48 hours. The invasion cell numbers in PTL-treated groups were significantly less than the control group (P < 0.05), which indicated that PTL suppressed cell invasion dose-dependently. PTL downregulated Bcl-2 and upregulated Bax expression. No change was found on Bad The underlying mechanism of PTL was also explored in the study. The activation of several apoptosis-related proteins Erismodegib concentration may contribute to PTL-induced apoptosis.

In Bcl-2 family members, the expression of Bcl-2, Bax and Bad after PTL treatment for 48 hours were detected by Western blotting (Fig. 5A). PTL obviously decreased the protein expression of antiapoptotic Bcl-2 and increased the protein expression of proapoptotic Bax in the BxPC-3 cells after being treated with indicated concentrations. No change was found on Bad. Therefore, the susceptibility to PTL-induced apoptosis might be attributable to the imbalance of Bcl-2/Bax (Fig. 5B). Figure 5 Apoptosis-related protein expression Monoiodotyrosine after PTL treatment for 48 hours. (A) PTL decreased Bcl-2 expression and induced Bax expression. No obvious change was observed on Bad; (B) Bcl-2/Bax ratio was decreased significantly with the increasing concentration of PTL; (C) Activation of caspase-9 and caspase-3 after PTL treatment. Effect of PTL at various concentrations on caspase-9 and caspase-3 expression Data have showed many anticancer agents are capable of initiating the caspase activation and inducing apoptosis [14]. Hence the caspase cascade in PTL-induced effect was also analyzed. After PTL treatment at indicated concentrations for 48 hours, Caspase-9 and Pro-caspase-3 expressions of BxPC-3 cell were explored (Fig. 5C). The dose-dependent proteolytic cleavage of caspase-9 was detected.

All subjects continued their previous therapy (e.g.,

topical tacrolimus or corticosteroids), only substituting the barrier-repair emollient for their previous moisturizer. Follow-up SCORAD scores improved significantly in 22 of 24 patients by 3 weeks, with further progressive improvement in all patients between 6 and 20 or 21 weeks. TEWL, which was elevated selleck chemicals over the involved and uninvolved areas at study entry, decreased in parallel with SCORAD scores and continued to decline even after the SCORAD scores plateaued. Stratum corneum integrity and hydration also improved significantly during therapy. The ultrastructure of the stratum corneum following treatment with the ceramide-dominant emollient revealed extracellular lamellar membranes, which were largely absent in baseline stratum corneum samples.

The authors concluded that a ceramide-dominant barrier-repair emollient represents a safe and useful adjunct to the treatment of childhood AD. EpiCeram® consists of a specific combination of ceramides, cholesterol, and fatty acids (in the ratio of 3:1:1), which mimic those naturally found in the skin [27, 28]. Recent studies have shown that EpiCeram® has efficacy similar to that of a mid-potency topical corticosteroid but has a more favorable safety profile [27, 28]. However, those studies did not report objective measurements to demonstrate the efficacy mTOR inhibitor of treatment. Hon et al. [29] studied skin hydration and TEWL on the forearm and determined the SCORAD score, Nottingham Eczema Severity Score (NESS), CDLQI, and amounts of emollient and cleanser used over a 2-week period

in consecutive new patients seen at the pediatric skin clinic. Patients with AD had significantly Liothyronine Sodium greater TEWL and less skin hydration at the studied sites. Although both skin dryness and skin hydration were improved, there was no significant improvement in the SCORAD score or TEWL after 2 weeks. In terms of GAT, three quarters of patients with AD and controls rated the combination of the cream and cleanser as good or very good. The authors concluded that liberal use of emollients and bathing cleanser alone does not seem to alter disease severity or TEWL within 2 weeks, implying that additional treatments are necessary to manage AD [29]. In another study, Hon et al. [13] recruited 33 patients with AD to study the clinical and biophysiological effects of twice-daily application of a pseudoceramide-containing cream. Four weeks after the patients started using the pseudoceramide cream, their skin hydration had improved significantly. There was no deterioration in TEWL, eczema severity, or quality of life in these patients. The pseudoceramide cream improved skin hydration but not eczema severity or quality of life over 4 weeks of use [13, 30].

Recently, immunohistochemical analysis showed that hypoxia-inducible factor 1 alpha (HIF-1alpha) expression levels were significantly higher in CCC than in other histological types of ovarian cancers [57]. Upstream target of HIF-1alpha, mammalian target of rapamycin (mTOR), was also reported to be up regulated in CCC [58, 59], which was selected for molecular target of CCC. There are two international collaborating studies led by Gynecologic Oncology Group (GOG) to evaluate efficacy of molecular targeting agents for CCC of the ovary [60, 61]. It is true that there existed GSK1120212 concentration super-responders

against molecular targeting agents in the patients with CCC. Consequently, further studies to evaluate these new drugs should include biomarker analysis to predict response or adverse effect for clinical application. Conclusions CCC has unique characteristics among ovarian cancers. We have to deal with the tumor using completely different techniques of treatment modality in terms with surgery and chemotherapy. Especially, we have to focus on histology-specific features of molecular pattern. We hope

the day will come when CCC tumors would be easily handled by the selection of effective surgery and chemotherapy including molecular targeting agents. References 1. Takeshima N, Hirai Y, Umayahara K, et al.: Lymph node Selinexor clinical trial metastasis in ovarian cancer: difference between serous and non-serous primary tumors. Gynecol Oncol 2005, 99:427–431.PubMedCrossRef 2. Di Re F, Fontanelli R, Raspagliesi F, et al.: Pelvic and para-aortic lymphadenectomy Protein kinase N1 in cancer of the ovary. Baillieres Clin Obstet Gynaecol 1989, 3:131–142.PubMedCrossRef 3. Petru E, Lahousen M, Tamussino K, et al.: Lymphadenectomy in stage I ovarian cancer. Am J Obstet Gynecol 1994, 170:656–662.PubMed 4. Onda T, Yoshikawa H, Yokota H, et al.: Assessment of metastases to aortic and pelvic lymph nodes

in epithelial ovarian carcinoma, A proposal for essential sites for lymph node biopsy. Cancer 1996, 78:803–808.PubMedCrossRef 5. Baiocchi G, Grosso G, di Re E, et al.: Systematic pelvic and paraaortic lymphadenectomy at second-look laparotomy for ovarian cancer. Gynecol Oncol 1998, 69:151–156.PubMedCrossRef 6. Suzuki M, Ohwada M, Yamada T, et al.: Lymph node metastasis in stage I epithelial ovarian cancer. Gynecol Oncol 2000, 79:305–308.PubMedCrossRef 7. Sakuragi N, Yamada H, Oikawa M, et al.: Prognostic significance of lymph node metastasis and clear cell histology in ovarian carcinoma limited to the pelvis (pT1M0 and pT2M0). Gynecol Oncol 2000, 79:251–255.PubMedCrossRef 8. Negishi H, Takeda M, Fujimoto T, et al.: Lymphatic mapping and sentinel node identification as related to the primary sites of lymph node metastasis in early stage ovarian cancer. Gynecol Oncol 2004, 94:161–166.PubMedCrossRef 9. Takano M, Kikuchi Y, Yaegashi N, et al.

Food Chem 2010, 122:1083–1088.CrossRef 22. Vuorela S, Kreander K, Karonen M, Nieminen R, Hämäläinen M, Galkin A, Laitinen L, Salminen JP, Moilanen E, Pihlaja K, Vuorela H, Vuorela P, Heinonen M: Preclinical evaluation of rapeseed, raspberry, and pine bark phenolics for health related effects. J Agric Food Chem 2005, 53:5922–5931.PubMedCrossRef 23. Marino A, Bellinghieri V, Nostro A, Miceli N, Taviano MF, Guvenc A, Bisignano G: In vitro effect of branch extracts of Juniperus species from Turkey on Staphylococcus

aureus biofilm. FEMS Immunol Med Microbiol 2010, 59:470–476.PubMed 24. Miceli N, Trovato A, Marino A, Bellinghieri V, Melchini A, Dugo P, Cacciola F, Donato P, Mondello L, Guvenc A, De Pasquale R, Taviano MF: Phenolic composition and biological activities of Juniperus drupacea Labill. Berries from Turkey. Food Chem Toxicol 2011, buy GSI-IX 49:2600–2608.PubMedCrossRef 25. Mandalari G, Bisignano C, D’Arrigo M, Ginestra G, Arena A, Tomaino A, Wickham MS: Antimicrobial potential of polyphenols extracted from almond skins. Lett Appl Microbiol 2010, 51:83–89.PubMed 26. Arena A, Bisignano C, Stassi G, Mandalari G, Wickham MSJ, Bisignano G: Immunomodulatory and antiviral activity of almond skins. Immunol Lett

2010, 132:18–23.PubMedCrossRef 27. Mandalari G, Bisignano C, Genovese T, Mazzon find more E, Wickham MS, Paterniti I, Cuzzocrea S: Natural almond skin reduced oxidative stress and inflammation in an experimental selleck screening library model of inflammatory bowel disease. Int Immunopharmacol 2011, 11:915–924.PubMedCrossRef 28. Faundez G, Troncoso M, Figueroa G: cagA and vacA in strains of Helicobacter pylori from ulcer

and non-ulcerative dyspepsia patients. BMC Gastroenterol 2002, 2:20.PubMedCrossRef 29. Clinical and Laboratory Standards Institute: Performance standards for antimicrobial susceptibility testing; twentieth informational supplement. M100-S22. Wayne: PA: CLSI; 2012. 30. Martini S, Bonechi C, Rossi C, Figura N: Increased susceptibility to resveratrol of Helicobacter pylori strains isolated from patients with gastric carcinoma. J Nat Prod 2011, 74:2257–2260.PubMedCrossRef 31. Liu W, Hsu C, Yin M: In vitro anti- Helicobacter pylori activity of diallyl sulphides and protocathecuic acid. Phytother Res 2008, 22:53–57.PubMedCrossRef 32. Funatogawa K, Hayashi S, Shimomura H, Yoshida T, Hatano T, Ito H, Hirai Y: Antibacterial activity of hydrolysable tannins derived from medicinal plants against Helicobacter pylori . Microbiol Immunol 2004, 48:251–261.PubMed 33. Toyoda T, Tsukamoto T, Mizoshita T, Nishibe S, Deyama T, Takenata Y, Hirano N, Tanaka H, Takasu S, Ban H, Kumagai T, Inada K, Utsunomiya H, Tatematsu M: Inhibitory effect of nordihydroguaiaretic acid, a plant lignan, on Helicobacter pylori -associated gastric carcinogenesis in Mongolian gerbils. CancSci 2007, 98:1689–1695. 34. Xiao Z-P, Shi D-H, Li H-Q, Zhang L-N, Xu C, Zhu H-L: Polyphenols based on isoflavones as inhibitors of Helicobacter pylori urease.

Probiotics Antimicrob Proteins 2010, 2:98–103.CrossRef 32. Naghmouchi K, Belguesmia Y, Baah J, Teather R, Drider D: Antibacterial activity of class I and IIa bacteriocins combined with polymyxin E against resistant variants of Listeria monocytogenes and

Escherichia coli . Res Microbiol 2011, 162:99–107.PubMedCrossRef 33. Giacometti A, Cirioni O, Barchiesi F, Fortuna M, Scalise G: In vitro activity of cationic peptides alone and in combination with clinically used antimicrobial agents against Pexidartinib clinical trial Pseudomonas aeruginosa . J Antimicrob Chemother 1999, 44:641–645.PubMedCrossRef 34. Oshima S, Rea MC, Lothe S, Morgan S, Begley M, O’Connor PM, Fitzsimmons A, Kamikado H, Walton R, Ross RP, Hill C: Efficacy of organic acids, bacteriocins, and the lactoperoxidase system in inhibiting the growth selleckchem of Cronobacter spp. in rehydrated infant formula. J Food Prot 2012, 75:1734–1742.PubMedCrossRef 35. Piper C, Draper LA, Cotter PD, Ross RP, Hill C: A comparison of the activities of lacticin 3147 and nisin against drug-resistant Staphylococcus aureus and Enterococcus species. J Antimicrob Chemother 2009, 64:546–551.PubMedCrossRef 36. Naghmouchi K, Baah J, Hober D, Jouy E, Rubrecht C, Sane F, Drider D: Synergistic effect between colistin and bacteriocins in controlling Gram-negative pathogens and their potential

to reduce antibiotic toxicity in mammalian epithelial cells. Antimicrob Agents Chemother 2013, 57:2719–2725.PubMedCrossRef 37. Gales AC, Reis AO, Jones RN: Contemporary assessment of antimicrobial susceptibility testing methods for polymyxin B and colistin: review of available interpretative criteria and quality control CYTH4 guidelines. J Clin Microbiol 2001, 39:183–190.PubMedCrossRef 38. Hermsen ED, Sullivan CJ, Rotschafer JC: Polymyxins: pharmacology, pharmacokinetics, pharmacodynamics,

and clinical applications. Infect Dis Clin North Am 2003, 17:545–562.PubMedCrossRef 39. Klostermann K, Crispie F, Flynn J, Meaney WJ, Ross RP, Hill C: Efficacy of a teat dip containing the bacteriocin lacticin 3147 to eliminate Gram-positive pathogens associated with bovine mastitis. J Dairy Res 2010, 77:231–238.PubMedCrossRef 40. Ryan MP, Meaney WJ, Ross RP, Hill C: Evaluation of lacticin 3147 and a teat seal containing this bacteriocin for inhibition of mastitis pathogens. Appl Environ Microbiol 1998, 64:2287–2290.PubMed 41. Shpigel NY, Elazar S, Rosenshine I: Mammary pathogenic Escherichia coli . Curr Opin Microbiol 2008, 11:60–65.PubMedCrossRef 42. Schukken Y, Chuff M, Moroni P, Gurjar A, Santisteban C, Welcome F, Zadoks R: The “”other”" Gram-negative bacteria in mastitis: Klebsiella, Serratia, and more. Vet Clin North Am Food Anim Pract 2012, 28:239–256.PubMedCrossRef 43. Hogan JS, Smith KL: A practical look at environmental mastitis. Comp Cont Educ Pract 1987, 9:F341-F346. 44. Arduino RC, Murray BE, Rakita RM: Roles of Antibodies and Complement in Phagocytic Killing of Enterococci. Infection and Immunity 1994, 62:987–993.

Parental training is considered a very important part of the treatment for children with ADHD and conduct

disorders. A different, more complicated situation exists in adult psychiatry. In some (unfortunately few) departments of psychiatry, family therapy is central to the treatment plan for persons suffering from mental disorders. At numerous other psychiatric wards, the family paradigm is not an important part of the treatment plan, and the family is only offered psycho-education. However, one may say that buy STA-9090 family is important to the success of treatment and represents an important third point in the triangle: patient—treating institution (represented by the physician)—family. As far as social services are concerned, family therapy is a well-developed practice in social services for children and adolescents. The growing interest in the systemic approach,

and especially in systemic consultation, can be observed within the education system. This interest results from the fact that the former model used by psychologists and pedagogues employed in the education system has proven ineffective in dealing with school, family, and other systemic problems. Many staff members of the Psychological PLX3397 cost and Pedagogical Counseling Centers (Poradnie Psychologiczno-Pedagogiczne) who work in the Ministry of Education received training in family therapy. It is worth emphasizing that some of those centers changed their structure and became psychotherapeutic institutions selleck chemicals llc offering, among other services, family therapy. Parental skills training is offered to parents with children with conduct disorders and children suffering from ADHD; systemic therapy is also offered to other children. Family therapy for adults is available and offered mainly in rehabilitation

centers. In 2008, there was an attempt to describe the institutional context for family therapy practice in Poland. To accomplish this goal, 396 questionnaires were sent to psychiatric, psychotherapeutic, and psychological institutions, as well as to individuals. The survey concerned, among other things, specialized education in family therapy, obtaining a psychotherapist certificate, the availability of regular supervision, approaches used, cooperation with other professionals, and the types of problems presented by clients (Józefik and Maryon 2008). In the end, 40 responses were received from the institutions. In 31 of them, family therapy was free of charge for clients: 25 were financed by the municipality, 5 were financed through social services, and 1 was financed by a non-profit foundation. The other 9 institutions offered family therapy for a fee. In the organizations that sent responses, therapists worked in teams of 2–12 people, with 5–8 members on average. There were a total of 185 therapists conducting family therapy.

Both mutants could swarm on 1.5% agar: swarms were 32% and 89% the level of the control for G21V and L22V, respectively as shown in Figure 6B. Both strains swarmed poorly on 0.3% agar, 3% and 37% that of the control for G21V and

L22V, respectively, which suggests that both mutations exert stronger effects on S-motility than on A-motility. Figure 6 Mutants with activating mutations display defects in one or both motility systems. MglA alleles which were made to resemble activating mutations in Ras displayed decreased or check details absent motility in a complementing strain. Mutations shown in this figure include MxH2361 (G21V), MxH2359 (L22V), MxH2357 (P80A), MxH2320 (Q82A) and MxH2319 (Q82R). See Figure 2 legend. Cells containing MglAG21V could Trichostatin A neither move individually on a 1.5% agarose surface nor in 0.5% MC (videomicroscopy, Table 1), although stable MglA was produced and some flares were observed at the colony edge (third panel, Figure 6C). In contrast, videomicroscopy showed that the L22V mutant glided well on agarose (90% of the control) and showed

speeds in methylcellulose of 71% of the control (Table 1). Reversals occurred less frequently in the L22V mutant (1 in 20.6 min, compared to 1 in 14.8 min for the control) in both agarose and in MC (1 in 12.0 min, compared with 1 in 10.8 min for control). Although these results would seem to contradict the swarming assay, we observed a density-dependent effect on motility in the microscopic assays. When cells were in contact, both G21V and L22V speeds increased and more closely correlated with their success in swarming assays. The proline in PM3, P80, is conserved in proteins

closely related to MglA as well as distant relatives LepA, Obg, Era and YihA. Many eukaryotic GTPases, such as those in the Rho, Ras and Rab families, contain an alanine in this position. The analogous residue A59 in Ha-Ras is involved in retaining GDP by preventing dissociation of the ligand by conformational change in Ha-Ras and mutation to threonine is considered an activating mutation [13]. To explore the possibility that substitution of the bulky 4��8C proline in MglA might improve its function, P80 was changed to alanine. Although the P80A mutant improves the PM3 motif match with most eukaryotic, as well as many prokaryotic GTPases such as FtsY, YchF, and TrmE, this mutation completely abolished MglA function in vivo despite the fact that stable MglA protein was made (Figure 6D). The P80A mutant was mot- and dev-. MglAQ82 mutants were expected to reduce the rate of GTP hydrolysis based on the effect of the analogous change in Ras (Q61). Initially Q82R was made to mimic known Ras mutants but this mutant allele failed to produce detectable MglA (Figure 6D) and the strain was nonmotile. Subsequently, Q82A was made to offset concerns that the charged arginine in this position inhibited folding of MglA.

In addition, Lü et al. calculated the band structure of a zigzag GNR with line defect [40]. They observed that the lowest conduction subband of this structure connects two inequivalent Dirac points with flat dispersion, which is reminiscent of the flat-bottomed subband of a zigzag GNR. Accordingly, a valley filtering device based on a finite length line defect in graphene was proposed.

It is easy to note that the effect of SB525334 the line defect in the zigzag GNRs has extensively discussed, but few works focused on the AGNRs with line defect. The main reason may be that the line defect can be extended along the zigzag GNRs. It should be certain that the line defect in the AGNRs plays a nontrivial role in the electron transport manipulation despite its terminated topology. With this idea, we, in this work, investigate the electron transport in an AGNR with line defect. We observe that the line defect induces Vemurafenib datasheet the abundant Fano effects and BIC phenomenon in the electron transport process, which is tightly dependent on the width of the AGNR. According to the numerical results, we propose such a structure to

be a promising candidate for electron manipulation in graphene-based material. Model and Hamiltonian We describe the structure of the AGNR with an embedded line defect using the tight-binding model with the nearest-neighbor approximation, i.e.: (1) where H C and H D are

the Hamiltonians of the AGNR and the line defect, respectively. H T represents the coupling between the AGNR and the defect. These three terms are written as follows: Here, the index i c (m d ) is the site coordinate in the AGNR (line defect), and 〈i c ,j c 〉 (〈m d ,n d 〉) denotes the pair of nearest neighbors. t 0 and t D are the hopping energies of the AGNR and line defect, respectively. ε c and ε d are the on-site energies in the AGNR and the line defect, respectively. t T denotes the coupling between the AGNR MRIP and line defect. With the help of the Landauer-Büttiker formula [41], the linear transport properties in this structure can be evaluated, i.e.: (2) T(ω) is the transmission probability, and ε F is the Fermi energy. The transmission probability is usually calculated by means of the nonequilibrium Green function technique or the transfer matrix method. In this work, we would like to use the nonequilibrium Green function technique to investigate the electron transport properties. For convenience, we divide the nanoribbon into three regions, i.e., the source (lead-L), the device, and the drain (lead-R). As a result, the transmission probability can be expressed as follows: (3) denotes the coupling between lead- L (R) and the device region, and Σ L/R is the self-energy caused by the coupling between the device and lead regions.

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