(B) Colony formation assay was used to measure cell proliferative

(B) Colony formation assay was used to measure cell proliferative capacity in MDA-MB-231 cells treated with control siRNA or BIRC5 siRNA. *, P < 0.05. Repressing LASP1 expression could inhibit migration of MDA-MB-231 cells To investigate the effect of LASP1 on selleck chemical the migration of TNBC cell, we evaluated the cell migratory capacity of MDA-MB-231 cells transfected with LASP1 siRNA (or control siRNA). The expression of LASP1 protein in the cells transfected with LASP1 siRNA was significantly decreased in comparison with that of cells transfected with control siRNA (Figure 5A), indicating that the expression of LASP1 was effectively inhibited by LASP1 siRNA. Subsequent studies

showed that the migratory capacity of cells transfected with LASP1 siRNA was significantly lower than that of cells treated with control siRNA (Figure 5B). Figure 5 Repressing LASP1 expression could

VX-680 inhibit migration of MDA-MB-231 cells. (A) Immunoblots of LASP1 protein in MDA-MB-231 cells treated with control siRNA or LASP1 siRNA. β-actin was used as a TSA HDAC price loading control. (B) Transwell migration assay was performed to detect the migratory capacity of MDA-MB-231 cells treated with control siRNA or LASP1 siRNA. *, P < 0.05. The inhibition of MDA-MB-231 cell proliferation by miR-203 is attenuated by the over-expression of BIRC5 To provide direct evidence that down-regulation of BIRC5 is required for the anti-tumorigenic effects of miR-203, we transfected MDA-MB-231 cells with pcDNA-BIRC5 and miR-203 precursor. We first confirmed that BIRC5 and miR-203 have been conducted into the cells (Figure 6A), then, we used colony formation assay to show that the inhibition of MDA-MB-231 cell proliferation by miR-203 could be partially rescued by BIRC5 up-regulated (Figure 6B). These data clearly indicate that the ectopic over-expression of BIRC5 could efficiently block the effect on proliferation caused by miR-203. Figure 6 Over-expression of BIRC5 could significantly attenuate the effect of miR-203 on the inhibition of MDA-MB-231 cell

proliferation. (A) BIRC5 protein expression was detected by western blot and normalized to β-actin protein ADP ribosylation factor levels. (B) Colony formation assay was performed to detect proliferative capacity in MDA-MB-231 cells. *, P < 0.05. The inhibition of MDA-MB-231 cell migration by miR-203 is attenuated by the over-expression of LASP1 To provide direct evidence that miR-203 inhibits the migration of TNBC cells through the LASP1-mediated signal pathway, we transfected MDA-MB-231 cells with miR-203 precursor and pcDNA-LASP1. We confirmed the effect of the transfection by western blot (Figure 7A). The migration assay showed that the over-expression of LASP1 could partially rescue the migratory capacity of MDA-MB-231 cells treated with the miR-203 precursor (Figure 7B). Figure 7 Over-expression of LASP1 significantly attenuated the effect of miR-203 on the inhibition of MDA-MB-231 cell migration.

The anaerobic test was a modified form of the Wingate test [20]

The anaerobic test was a modified form of the Wingate test [20]. The load on the ergometer platters, which was optimum for each athlete, was determined during a pilot study and amounted to 8.3% of BM on average, i.e. by 0.8 higher

than in the original. With this braking force, the athletes generated the greatest peak power. It consisted in pedaling for 30 seconds with maximal intensity using a mechanical bicycle ergometer Ergomedic 874E Crenigacestat datasheet manufactured by Monark. During the exercise, a computer recorded relative peak power (RPP) and relative total work (RTW), time to obtain peak power (toPP), time to maintain peak power (tuPP) and the fatigue index (FI). Graded test until fatigue A graded exercise test on a mechanical treadmill was carried out on the second day of the experiment, under similar ambient conditions.

After the determination of pre-exercise circulatory and respiratory indices, the subjects performed a 3-minute warm-up this website at the running speed of 2.3 m.s-1, and then the speed was increased by 0.5 m.s-1 ATM Kinase Inhibitor every three minutes. During the last 30 seconds of each loading segment, the subjects were taken blood samples from the earlobe in order to determine the lactate concentration in blood serum. The graded exercise was continued by the subjects until a subjective sensation of exhaustion. Using the apparatus of 919E type manufactured by Medikro, the indices of respiratory exchange were measured during the exercise every 30 seconds: tidal volume (TV), respiratory rate (F), minute ventilation (VE), minute oxygen uptake (VO2). Heart rate monitor VantageTM manufactured by Polar Electro was used for the measurements of heart rate (HR). Total time of exercise (t) and the distance (D) were also recorded. It was established based on a pilot study that the capillary blood samples used for Tau-protein kinase the determination of biochemical and morphological indices would be also taken from the earlobe three minutes after the exercise. This was the point when the highest lactate (La) concentration was found. All the exercise tests were performed in

an air-conditioned room in the Department of Physiology and Biochemistry of the Institute of Human Physiology. The project was approved by the Bioethical Committee at the Regional Medical Chamber (No. 76KBL/OIL/2008 of 17 September 2008). Special Judo Fitness Test Special Judo Fitness Test (SJFT) invented by one of the authors of the present study is an acknowledged tool of training control, implemented in many countries [11]. Visualized presentation was prepared at the University of Bath by Lance Wicks [21]. The test positively passed the statistic procedures determining the reliability and accuracy, and had normative data [11]. SJFT is a recognized tool used also in judo-related disciplines, such as ju-jitsu, hapkido etc. Statistical analysis The following descriptive statistics were calculated: mean, SD, median. Non-parametric methods were used, because not all parameters show normal distribution.

Biotechnology 1983, 9:184–191 22 Hanahan D: Studies

on

Biotechnology 1983, 9:184–191. 22. Hanahan D: Studies

on transformation of Escherichia coli with plasmids. J Mol Biol 1983,166(4):557–580.PubMedCrossRef 23. Rogers M, Ekaterinaki N, Nimmo E, Sherratt D: Analysis of Tn7 transposition. Mol Gen Genet 1986,205(3):550–556.PubMedCrossRef 24. Morehouse KA, Hobley L, Capeness M, Sockett RE: Three motAB Stator Gene Products in Bdellovibrio bacteriovorus Contribute to Motility of a Single Flagellum during Predatory and Prey-Independent Growth. J Bacteriol 2011,193(4):932–943.PubMedCrossRef 25. Evans KJ, Lambert C, Sockett RE: Predation by Bdellovibrio bacteriovorus HD100 requires type IV pili. J Bacteriol 2007,189(13):4850–4859.PubMedCrossRef Competing interests

The authors declare that they have no competing interests. NVP-LDE225 order Authors contributions RES designed the experiments and co-authored the manuscript. CL performed the RT-PCR and luminescence assays and co-authored the manuscript, RT Selleckchem Proteasome inhibitor constructed the mutants and performed RT-PCR, LH performed the electron microscopy and speed measurements. All authors read and approved the final manuscript”
“Background Salmonella enterica is a common cause of human gastroenteritis and bacteremia worldwide [1–3] and a wide variety of animals, particularly food animals, have been JNK-IN-8 price identified as reservoirs for non-typhoidal Salmonella[4]. Although approximately 2,600 serovars of Salmonella enterica have been identified, most human infections are caused by a limited number of serovars and in general these infections are self-limiting [1]. However, approximately 5% of patients infected with non-typhoidal Salmonella,

will develop bacteremia. The very young, elderly, and those with underlying disease are at a significantly higher risk for developing bacteremia when compared to patients with enteric salmonellosis. Bacteriaemic patients have higher rates of hospitalization, often have prolonged courses of illness and have higher case fatality rates [1, 5]. Worldwide, Salmonella enterica serovars Enteritidis and Typhimurium are consistently ranked as the two serovars most frequently associated with human disease [6]. However, these rankings may considerably vary by geographic region and may change over time. A recent study showed that in 2007, Demeclocycline Salmonella serovar Enteritidis accounted for 55% of all human Salmonella infections reported to the World Health Organization Global Foodborne Infections Network Country Data Bank [6]. In that same year, Salmonella serovar Enteritidis only accounted for 16% of human salmonellosis cases in Thailand [7]. In 2009, an observational study based on patient data from 11,656 Salmonella isolates collected between 2002 – 2007 estimated risk factors for the ten most common Salmonella serovars isolated from Thai patients [7]. In the study, 60.

tuberculosis-induced DNA fragmentation, as recommended by the man

tuberculosis-induced DNA fragmentation, as recommended by the manufacturer. Briefly, 1-3 days after infection, 48-well plates were centrifuged at 200 × g to sediment detached cells, the medium was discarded, and the cells were lysed. The lysate was subjected to antigen capture enzyme-linked immunosorbent assay learn more (ELISA) to measure free nucleosomes, and the optical density at 405 nm (OD405) was

read on a Victor2 plate reader (Wallac/Perkin Elmer, Waltham, MA). Triplicate wells were assayed for each condition. Staurosporine (Sigma) (1 μM, diluted in serum-free RPMI) was applied for 24 h as a positive control for DNA fragmentation. Caspase Inhibition The pan-caspase inhibitor, Q-VD-OPh (20 μM; Enzo Life Sciences AG, Lausen, Switzerland), was applied to

DCs 4 h prior to infection with H37Ra and replenished every 24 h throughout the duration of infection Caspase-Glo Assay Caspase 3/7 activity was measured using the luminescent Caspase-Glo assay system (Promega, Madison, WI). DCs were cultured in 96-well plates and the assays were carried out in a total volume of 200 μl. After equilibration to room temperature, Caspase-Glo selleckchem reagent was added to each well and gently mixed using a plate shaker at 300 rpm for 30 s. The plate was incubated at room temperature for 30 minutes and luminescence was then selleck chemicals llc measured

using a Victor2 plate reader. Laser Scanning Confocal Microscopy Following infection, DCs were fixed for 10 min (H37Ra) or 24 h (H37Rv) in 2% paraformaldehyde (Sigma), applied to glass slides and left to air dry overnight. The cells were then stained with modified auramine O stain for acid-fast bacteria and DC nuclei were counterstained with 10 μg/ml of Hoechst 33358. The slides were analysed using a Zeiss LSM 510 laser confocal microscope equipped with an Argon (488 nm excitation line; 510 nm Aspartate emission detection) laser and a diode pulsed solid state laser (excitation 561 nm; emission 572 nm long pass filter) (Carl Zeiss MicroImaging GmbH, Oberkochen, Germany). Images were generated and viewed using LSM Image Browser (Carl Zeiss MicroImaging). Flow Cytometry Dendritic cell surface markers were analysed by flow cytometry on a CyAn ADP flow cytometer (Dako/Beckman Coulter). Dendritic cells were infected with live H37Ra, or streptomycin-killed H37Ra at MOI 1 for 24 or 48 h. As a positive control for maturation, uninfected DCs were treated with LPS (Sigma; 1 μg/ml) for 24 h prior to staining for flow cytometry. Cells were incubated with antibodies for 30 min and fixed with 2% paraformaldehyde for at least 1 h prior to flow cytometry.

Archer C, Levy AR, McGregor M (2003) Value of routine preoperativ

Archer C, Levy AR, McGregor M (2003) Value of routine preoperative chest x-rays: a meta-analysis. Can J Anaesth 40:1022–1027CrossRef 68. Joo HS,

Wong J, Naik VN, Savoldelli GL (2005) The value of screening preoperative chest x-rays: a systematic review. Can J Anaesth 52:568–574CrossRefPubMed 69. Williams-Russo P, Charlson ME, MacKenzie CR, Gold JP, Shires GT (1992) Predicting postoperative pulmonary complications: is it a real problem? Arch Intern Med 152:1209–1213CrossRefPubMed 70. this website Lawrence VA, Dhanda R, Hilsenbeck SG, Page CP (1996) Risk of pulmonary complications after elective abdominal surgery. Chest 110:744–750CrossRefPubMed 71. Milledge JS, Nunn JF (1975) Criteria of fitness for anaesthesia in patients with chronic obstructive lung disease. BMJ 3:670–673CrossRefPubMed 72. Stein M, Koota GM, Simon M, Frank HA (1962) Pulmonary selleck inhibitor evaluation of surgical patients. JAMA 181:765–770PubMed 73. Kearney DJ, Lee TH, Reilly JJ, DeCamp MM, Sugarbaker DJ (1994) Assessment of operative risk in patients undergoing lung resection: importance of predicted pulmonary function.

Chest 105:753–759CrossRefPubMed 74. Lawrence VA, Cornell JE, Smetana GW (2005) Strategies to reduce postoperative pulmonary complications after noncardiothoracic surgery: Combretastatin A4 chemical structure systematic review for the American College of Physicians. Ann Intern Med 144:596–608 75. Castillo R, Haas A (1985) Chest physical therapy: comparative efficacy of preoperative and postoperative in the elderly. Arch Phys Med Rehabil 66:376–379PubMed 76. Thomas JA, McIntosh JM (1994) Are incentive spirometry, intermittent positive pressure breathing, and deep breathing exercises effective in the prevention of postoperative pulmonary complications after upper abdominal surgery? A systematic overview and meta-analysis. Phys Ther 74:3–16PubMed 77. Brooks-Brunn JA (1995) Postoperative atelectasis and pneumonia. Heart Lung 24:94–115CrossRefPubMed 78. Stock MC, Downs JB, Gauer PK, Alster JM, Imrey

PB (1985) Prevention of postoperative pulmonary complications with CPAP, incentive spirometry, and conservative therapy. Chest 87:151–157CrossRefPubMed 79. Squadrone V, Coha M, Cerutti E et al (2005) Continuous positive airway pressure for treatment of postoperative hypoxemia: a randomized controlled trial. JAMA 293:589–595CrossRefPubMed 80. Geerts WH, Teicoplanin Bergqvist D, Pineo GF, Heit JA, Samama CM, Lassen MR, Colwell CW (2008) Prevention of venous thromboembolism: American College of Chest Physicians Evidence-Based Clinical Practice Guidelines (8th Edition). Chest 133:381S–453SCrossRefPubMed 81. Morrison RS, Chassin MR, Siu AL (1998) The medical consultant’s role in caring for patients with hip fracture. Ann Intern Med 128:1010–1020PubMed 82. Hull RD, Pineo GF, Francis C et al (2000) Low-molecular-weight heparin prophylaxis using dalteparin in close proximity to surgery vs warfarin in hip arthroplasty patients: a doubleblind, randomized comparison. Arch Intern Med 160:2199–2207CrossRefPubMed 83.

In this study, a Sb-doped ZnO

In this study, a Sb-doped ZnO microrod array was successfully grown on an Al-doped n-type ZnO thin film by electrodeposition. Strong violet luminescence, originated from free electron-to-acceptor level transitions, was identified by temperature-dependent selleck kinase inhibitor photoluminescence measurements. This acceptor-related transition was attributed to substitution of Sb dopants for Zn sites, instead of O sites, to form a complex with two Zn vacancies (VZn), the SbZn-2VZn complex. This

SbZn-2VZn complex has a lower formation energy and acts as a shallow acceptor which can induce a strong violet luminescence. ZnO homojunction diode made with Sb-doped ZnO and Al-doped ZnO exhibits the expected p-n diode characteristic on the current-voltage (I-V) measurement and confirms that the Sb-doped ZnO microrod array is p-type and can be

ATM Kinase Inhibitor fabricated successfully using the electrodeposition method. Finally, the photoresponse of the ZnO p-n diode operating at an increased Selleck EPZ 6438 reverse bias shows a good optical response and high photocurrent gain, indicating that it can be a good candidate for use as an ultraviolet photodetector. Methods A Sb-doped ZnO microrod array was electrodeposited on a patterned Al-doped n-type ZnO thin film at 98°C for 1 h [15]. The array pattern was fabricated on the ZnO thin film by optical lithography method. The reaction solution for the growth of the microrod

array was a mixture of 0.05 M zinc nitrate (Zn(NO3)2·6H2O), 0.05 M hexamethylenetetramine (C6H12N4), and 0.05 g antimony acetate (Sb(CH3COO)3). The conditions for electrodeposition were optimized at I = 10 mA and V = 3.1 V. Ohmic contacts on the n-type ZnO thin film and on the Sb-doped ZnO microrod array were fabricated by depositing aluminum and gold antimony (AuSb), respectively, for the electrical characterization. The surface morphology and the crystalline structure of the sample were examined using a selleck compound scanning electron microscope (SEM; HITACHI S-2400, Chiyoda-ku, Japan) and by X-ray diffraction (XRD; PANalytical X’Pert PRO, Almelo, The Netherlands), respectively. The chemical and elemental identification on the surface was carried out by X-ray photoelectron spectroscopy (XPS). A He-Cd laser at the wavelength of 325 nm was used for the photoluminescence (PL) measurement. Keithley 236 and 4200-SCS (Cleveland, OH, USA) were used for the characteristic I-V measurement. To study the photoresponse of our ZnO homojunction device, we employed a xenon arc lamp (LHX150 08002, Glasgow, UK) as a variable-wavelength light source. The monochromatic light was selected using an iHR-320 monochromator (HORIBA Scientific, Albany, NY, USA) and irradiated on the sample. The beam line of 365 nm was selected in the photocurrent measurement.

In both cases, differences post-match did not reach statistical s

In both cases, differences post-match did not reach A-1210477 supplier statistical significance. Other conflicting findings have been reported for these enzymes; no increase following exercise was found in the concentration of GPx [34–36], or SOD [35, 37, 38]. Clearly, these results are likely to depend on the time of sampling, the type of isoenzyme measured (in the case of SOD), the specific sample (plasma, erythrocytes, lymphocytes, neutrophils), the kind

of exercise performed, as well as the duration and intensity of exercise, which varies considerably across studies. Furthermore, we found that SOD activity was closely associated with vitamin B6 levels, since players who did not meet with the recommended intake of vitamin B6 showed lower SOD activity immediately post-match. Similar findings were recently reported in rats who when fed with a B6-deficient diet MCC950 presented lower concentration of SOD activity in kidney [39].

A more pronounced decrease in SOD activity was earlier reported in rats fed a vitamin B6 deficient diet after exercise-induced oxidative stress [40]. Soccer has been described as an aerobic-anaerobic sport in which players’ movements can involve eccentric muscle contractions resulting in muscle fiber and therefore cell breakdown. Some markers, such as CK and LDH, have been used as a way to indicate the grade of cell damage, especially after playing a sport [6, 41–44], since microfiber breakdown releases cell content. HDAC inhibitor Thus, serum concentrations of skeletal muscle enzymes constitute a marker of the functional status of muscle tissue and varies widely in both pathological and physiological conditions. Thus, monitoring the concentrations of these markers can help to avoid tissue damage [45]. Although it

has long been recognized that there is a close association between dietary carbohydrate intake, muscle glycogen concentration and endurance capacity, these relationships with CK activity are still unknown. In this regard, our study demonstrates PD184352 (CI-1040) that higher carbohydrate intake is associated with a diminished serum concentration of CK and LDH at rest. Several studies have investigated the effect of carbohydrates on the physiological effect induced by exercise, mostly during recovery. For example, after eccentric exercise, no significant effects were found after consuming a higher proportion of carbohydrates [46]. However, muscle recovery cannot be evaluated by changes in serum CK concentrations, as there is no correlation between serum enzyme leakage and muscular performance impairment after exercise [47]. Nevertheless, total creatine kinase levels have been found to depend on age, gender, race, muscle mass, physical activity and climatic condition, and after exercise, CK activity in serum has been found to depend on the level of training [48].

g , Sellers et al 1997; Hubbard et al 2001; Tardieu 2003; Buckl

g., Sellers et al. 1997; Hubbard et al. 2001; Tardieu 2003; Buckley 2005). Even mild water deficits, when relative water content remains above 70%, primarily cause limitation to carbon dioxide uptake because of stomatal closure. With greater water deficits, direct inhibition ARRY-438162 of photosynthesis occurs (Gupta and Berkowitz 1988; Smirnoff 1993). Phloem is responsible for the transport of photosynthates such as

sucrose from leaves to the rest of the plant. If unloading is inhibited photosynthesis will be decreased. Therefore, there is a strong interrelationship between photosynthesis activity/CO2 assimilation, plant water status, and xylem and phloem transport/hydraulic conductance (Daudet et al. 2002). Although these principles are now well known, the dynamics of the interrelationship and integration between these processes on plant level is still lacking. What we need is to be able to measure in intact plants phloem and xylem flow in relation to water content in the surrounding tissues (the storage pools), under normal

and under water limiting or even stress conditions 4EGI-1 cell line (e.g., drought or as a function of phloem loading/unloading mechanisms due to e.g., anoxia), in relation to photosynthesis activity. MRI methods and dedicated hardware have been presented to measure xylem and phloem water transport in relation to water content in different storage tissues (bark, cambial zone, xylem, and parenchyma) non-invasively in the stem of intact plants

(Van As 2007; Van As and Windt 2008). In addition, portable NMR (non-spatially resolved) is becoming available for Celecoxib water content measurements in leaves (Capitani et al. 2009). These NMR and MRI methods can be combined with measurements of photosynthesis learn more activity, e.g., monitoring by PAM techniques. In this review, we introduce these NMR and MRI methods and discuss them in relation to spatial and temporal resolution and (sub)cellular water content. Imaging principles and partial volume effects In a homogeneous main magnetic field B 0, equal spins (e.g., protons of the water molecules) have identical Larmor precession frequency, and a single resonance line in the frequency spectrum is observed at $$ \nu_0 = (\gamma/2\pi )B_0 $$ (1) γ is the gyromagnetic ratio that is a characteristic property for each type of spin bearing nuclei. For mobile (liquid) molecules the resonance line is Lorenzian shaped with a width at half maximum inversely proportional to the T 2, the spin–spin or transverse relaxation time.

Therefore, increasing peak bone mass in young people during the t

Therefore, increasing peak bone mass in young people during the time of skeletal maturation may

be the ‘best bet’ primary prevention strategy to reduce the likelihood of this disease [6]. While bone and body size have been identified NVP-BSK805 as the main determinants of bone mineral content (BMC) [7], physical activity (PA), nutritional factors, sex hormones and drugs have also been found to play a role in bone mineralization [6–8]. Positive relationships between dairy product intake and total BMC and BMD have been reported in women aged 18–50 y [6, 9]. However, it is uncertain which nutrient or combination of nutrients is responsible for changes in bone mass when dairy products are consumed because protein, calcium, phosphorus and vitamin D are known to be associated with bone health [6].

There is limited evidence of an effect of dietary calcium intake on BMC in children [10], young MEK inhibitor side effects women aged 19–35 y [11] and perimenopausal women aged 45 to 58 y with amenorrhoea for 2–24 months [12]. In adolescents aged 12 to 16 y [8], dietary calcium had no effect on BMC [8]. Physical activity (PA) on the other hand, has been shown to contribute to bone mass in many studies [10, 11, 13–16]. For example, BMC was found to be higher in the dominant arm of female tennis players [14] and in pre- and early-pubertal children with the highest levels of habitual PA [10] or involvement in a 2-year p38 MAPK inhibitors clinical trials school-based exercise program [5]. A study with 2384 young men attending the mandatory tests for selection to compulsory military service in Sweden found that history of regular physical was the strongest predictor and could explain 10.1% of the variation in BMD [17]. Type of PA has also been shown ZD1839 datasheet to contribute to bone mineralization. Whereas vigorous-intensity PA,

including resistance training programs and high-impact exercise has been shown to influence bone mass in some studies [7, 15, 18–20], others have shown that a minimum intake of calcium seems to be essential for PA to have an impact on bone mass [4, 21]. In contrast, strength training 3 d/wk for 12 months had no benefit on bone mineralization in postmenopausal women [21] and there was no association between bone mineralization and level and frequency of sports participation in adolescents aged 12 to 16 y [8]. Calcium and weight-bearing PA have been suggested to have their greatest effect early in life [4, 16, 22] and with consistently high calcium intake [4, 21, 23]. The recommended dietary intake (RDA) of calcium for men aged 19–30 y is 1000 mg/d [24] with most young men able to meet the RDA by consuming at least three servings of milk, cheese or yogurt daily. In Australia, the median intake of calcium in men 19–24 y was only 961.5 mg/d [25].

References 1 Galyov

EE, Brett

References 1. Galyov

EE, Brett 4EGI-1 purchase PJ, DeShazer D: Molecular insights into Burkholderia pseudomallei and Burkholderia mallei pathogenesis. Annu Rev Microbiol 2010, 64:495–517.PI3K Inhibitor Library PubMedCrossRef 2. Jones AL, Beveridge TJ, Woods DE: Intracellular survival of Burkholderia pseudomallei. Infect Immun 1996,64(3):782–790.PubMedCentralPubMed 3. Wiersinga WJ, Currie BJ, Peacock SJ: Melioidosis. N Engl J Med 2012,367(11):1035–1044.PubMedCrossRef 4. Wiersinga WJ, van der Poll T, White NJ, Day NP, Peacock SJ: Melioidosis: insights into the pathogenicity of Burkholderia pseudomallei. Nat Rev Microbiol 2006,4(4):272–282.PubMedCrossRef 5. Stevens MP, Haque A, Atkins T, Hill J, Wood MW, Easton A, Nelson M, Underwood-Fowler C, Titball RW, Bancroft GJ, Galyov EE: Attenuated virulence and protective efficacy of a Burkholderia pseudomallei bsa type III secretion mutant in murine models of melioidosis. Microbiology 2004,150(Pt 8):2669–2676.PubMedCrossRef 6. Warawa J, Woods DE: Type III secretion system cluster 3 is required for maximal virulence of Burkholderia pseudomallei in a hamster infection model. FEMS Microbiol Lett 2005,242(1):101–108.PubMedCrossRef 7. Lee YH, Chen Y, Ouyang

X, Gan YH: Identification of tomato plant as a novel host model for Burkholderia pseudomallei. BMC Microbiol 2010, 10:28.PubMedCentralPubMedCrossRef 8. Burtnick MN, Brett PJ, Nair V, Warawa JM, Woods DE, Gherardini www.selleckchem.com/products/apo866-fk866.html FC: Burkholderia pseudomallei type III secretion system mutants exhibit delayed vacuolar escape phenotypes in RAW 264.7 murine macrophages. Infect Immun 2008,76(7):2991–3000.PubMedCentralPubMedCrossRef 9. Stevens MP, Wood MW, Taylor LA, Monaghan P, Hawes P, Jones PW, Wallis TS, Galyov EE: An Inv/Mxi-Spa-like type III protein

secretion system in Burkholderia pseudomallei modulates intracellular behaviour of the pathogen. Mol Microbiol 2002,46(3):649–659.PubMedCrossRef 10. Sun GW, Lu J, Pervaiz S, Cao WP, Gan YH: Caspase-1 dependent macrophage death induced by Burkholderia Flucloronide pseudomallei. Cell Microbiol 2005,7(10):1447–1458.PubMedCrossRef 11. Miao EA, Mao DP, Yudkovsky N, Bonneau R, Lorang CG, Warren SE, Leaf IA, Aderem A: Innate immune detection of the type III secretion apparatus through the NLRC4 inflammasome. Proc Natl Acad Sci U S A 2010,107(7):3076–3080.PubMedCentralPubMedCrossRef 12. Kwuan L, Adams W, Auerbuch V: Impact of host membrane pore formation by the Yersinia pseudotuberculosis type III secretion system on the macrophage innate immune response. Infect Immun 2013,81(3):905–914.PubMedCentralPubMedCrossRef 13.