J Bone Miner Res 21(6):836–844PubMedCrossRef 9 Ward KA, Das G, R

J Bone Miner Res 21(6):836–844PubMedCrossRef 9. Ward KA, Das G, Roberts SA, et al (2010) A randomized, controlled trial of vitamin D supplementation upon musculoskeletal health in postmenarchal females. J Clin Endocrinol

Metab. Jul 14 10. Houghton LA, Vieth R (2006) The case against ergocalciferol (vitamin D2) as a vitamin supplement. Am J Clin Nutr 84(4):694–697PubMed 11. Arunabh S, Pollack S, Yeh J, Aloia JF (2003) Body fat content and 25-hydroxyvitamin D levels in healthy women. J Clin Endocrinol Metab 88(1):157–161PubMedCrossRef 12. Parikh SJ, Edelman M, Uwaifo GI et al (2004) The relationship between obesity and serum 1,25-dihydroxy vitamin D concentrations in healthy adults. J Clin Endocrinol Metab 89(3):1196–1199PubMedCrossRef

see more 13. Waldie KE, Poulton R, Kirk IJ, Silva PA (2000) The effects of pre- and post-natal sunlight exposure on human growth: evidence from the southern hemisphere. Early Hum Dev 60(1):35–42PubMedCrossRef 14. Sayers A, Tobias JH (2010) Fat mass exerts a greater effect on cortical bone mass in girls than boys. J Clin Endocrinol Metab 95(2):699–706PubMedCrossRef 15. Cheng S, Tylavsky F, Kroger H et al (2003) Association of low 25-hydroxyvitamin D concentrations with elevated parathyroid hormone concentrations and low cortical bone density in early pubertal and prepubertal Finnish girls. Am J Clin Nutr 78(3):485–492PubMed 16. Lehtonen-Veromaa MK, Mottonen TT, Nuotio IO, Irjala KM, Leino AE, Viikari JS (2002) Vitamin D and attainment of peak ZD1839 bone mass among peripubertal Finnish girls: a 3-y prospective study. Am J Clin Nutr 76(6):1446–1453PubMed 17. Tylavsky FA, Ryder KM, Li R et al (2007) small molecule library screening Preliminary findings: 25(OH)D levels and PTH are indicators of rapid bone accrual in pubertal children. J Am Coll Nutr 26(5):462–470PubMed 18. McKay HA, MacLean L, Petit M et al (2005) “Bounce at the bell”: a novel program of short bouts of exercise improves proximal femur

bone mass in early pubertal children. Br J Sports Med 39(8):521–526PubMedCrossRef 19. Cole ZA, Gale CR, Javaid MK et al (2009) Maternal dietary patterns during pregnancy and childhood bone mass: a longitudinal study. J Bone Miner Res 24(4):663–668PubMedCrossRef 20. Clark EM, Ness A, Tobias JH (2005) Social position affects bone mass in childhood through opposing actions on EVP4593 research buy height and weight. J Bone Miner Res 20:2082–2089PubMedCrossRef 21. Golding J, Pembrey M, Jones R (2001) ALSPAC — the Avon Longitudinal Study of Parents and Children: 1. Study methodology. Paediatr Perinat Epidemiol 15:74–87PubMedCrossRef 22. Morris N, Udrey J (1980) Validation of a self-administered instrument to assess stage of adolescent development. J Youth Adolesc 9:271–280CrossRef 23. Tobias JH, Steer CD, Mattocks C, Riddoch C, Ness AR (2007) Habitual levels of physical activity influence bone mass in 11 year-old children from the UK: findings from a large population-based cohort. J Bone Miner Res 22:101–109PubMedCrossRef 24.

J Appl Phys 1996, 80:3184–3190 CrossRef 64 Larcher D, Masquelier

J Appl Phys 1996, 80:3184–3190.CrossRef 64. Larcher D, Masquelier C, Bonnin D, Chabre Y, Masson V, Leriche JB, Tarascon JM: Effect of particle size on lithium intercalation into α-Fe 2 O 3 . J Electrochem Soc 2003, 150:A133-A139.CrossRef 65. Zhou W, Lin LJ, Wang WJ, Zhang LL, Wu QO, Li JH, Guo L: Hierarchial mesoporous hematite with “electron-transport channels” and its improved performances in photocatalysis and lithium ion batteries. J Phys Chem C 2011, 115:7126–7133.CrossRef 66. Cheng F, Huang KL, Liu SQ, Liu JL, Deng RJ: Surfactant carbonization to synthesize pseudocubic

α-Fe 2 O 3 /c nanocomposite SC75741 chemical structure and its electrochemical performance in lithium-ion batteries. Electrochim Acta 2011, 56:5593–5598.CrossRef 67. Sun B, Horvat J, Kim HS, Kim WS, Ahn J, Wang GX: Synthesis of mesoporous α-Fe 2 O 3 nanostructures for highly sensitive gas sensors and high capacity anode materials in lithium ion batteries. J Phys Chem C 2010, 114:18753–18761.CrossRef

68. Liu H, Wang GX, Park J, Wang J, Zhang C: Electrochemical performance of α-Fe 2 O 3 nanorods as anode material Caspase inhibitor for lithium-ion cells. Electrochim Acta 2009, 54:1733–1736.CrossRef 69. Reddy MV, Yu T, Sow CH, Shen ZX, Lim CT, Rao GVS, Chowdari BVR: α-Fe 2 O 3 nanoflakes as an anode material for Li-ion batteries. Adv Funct Mater 2007, 17:2792–2799.CrossRef 70. Pan QT, Huang K, Ni SB, Yang F, Lin SM, He DY: Synthesis of α-Fe 2 O 3 dendrites by a hydrothermal approach and their application in lithium-ion batteries. J Phys D Appl Phys 2009, 42:015417.CrossRef Competing interests The authors declare that they have no competing interests. Authors’ contributions WCZ provided guidance to XLC, XFL, and LYZ as he was the supervisor. WCZ and QZ wrote the paper. JQH conducted the research study on the Li-ion storage performance test. XLP conducted the surface area measurement. All authors read and approved the final manuscript.”
“Background Gold nanoparticles including nanoshells, nanocages, and nanorods have drawn increasing attention in photodynamic therapy (PDT), drug delivery, and diagnostic imaging field in recent years [1–5]. Among them, gold

nanorods Florfenicol (AuNRs) are of particular interest due to their unique optical properties. With the different aspect https://www.selleckchem.com/PD-1-PD-L1.html ratios and the resulting longitudinal surface plasmon resonance (SPR), AuNRs exhibit an absorption band in the near-infrared (NIR) region [6], which conduces to higher photothermal conversion and also shows significant biomedical application in view of the penetration of NIR light into biological tissues [7, 8]. Poly(N-isopropylacrylamide) (pNIPAAm) gel, as one of the most widely studied temperature-responsive polymers [9–11], undergoes phase transition in water when the temperature increases or decreases beyond its lower critical solution temperature (LCST; approximately 32°C) [12, 13]. Besides, its LCST can be tuned by the addition of a comonomer during polymerization [14, 15].

These results might help to unravel the intricate interactions

. These results might help to unravel the intricate interactions among plant root systems, root exudates, and rhizospheric microflora. Differentially expressed plant proteins under ratooning practice Our metaproteomic analysis showed that the 6 proteins (spot 12, succinate dehydrogenase; spot 13, phosphofructokinase; spots 16 and 35, glyceraldehyde-3-phosphate dehydrogenase and spot 32, fumarate hydratase 1) linked to the glycolysis (EMP) / tricarboxylic acid

(TCA) cycle and one protein Veliparib (spot 25, betaine aldehyde hydrogenase) involved in glycine, serine and threonine metabolism were highly expressed in the ratoon cane soil, as compared to the plant cane and control soils (Table 4). These proteins are probably associated with the release of root exudates from plants. Many root exudates (such as malate, fumarate, oxalate, malonate, citrate, aconitate, arginine, histidine and lysine) are mostly the intermediates of the TCA cycle or amino acid metabolism. Singh and Mukerji [34] suggested that these root exudates were the determinants of rhizospheric microbial biodiversity. Root exudates act as chemo-attractants that function to attract bacteria towards roots [35]. The qualitative and quantitative composition of root exudates is affected by various environmental factors (such as pH, soil type, oxygen status, nutrient availability, etc.) and the presence of microorganisms.

The up-regulation of these proteins involved in the carbohydrate and amino acid metabolism might be explained by a change in the composition of root exudates possibly resulting from soil disturbances Selleckchem FRAX597 which might be caused by ratooning. In this study, three proteins linked to plant stress/defense response (including spot 4, catalase; spot 23, PrMC3 and spot 27, heat shock 70

kDa protein) showed higher expression levels in the ratoon cane soil than in the plant cane and control soils (Table 4). Catalase and heat shock protein 70 (Hsp 70) have been proven to be critical Tyrosine-protein kinase BLK for various abiotic and biotic stress responses [36–38]. The above mentioned proteins are rapidly up-regulated in pathogen infection and play a central role in defense against pathogens [39, 40]. PrMC3 is a member of a family of proteins that all contain a Ser-hydrolase motif (GxSxG) and is similar to the tobacco protein selleck Hsr203J [41]. Hsr203J is rapidly and specifically expressed in the hypersensitive response to various pathogens in tobacco [42]. Furthermore, Zhou et al. [43] found that the gene expression of PrMC3 was up-regulated in the plant leaves infected by the bacterial pathogen Xanthomonas oryzae pv. Oryzicola. Therefore, the up-regulation of catalase, PrMC3 and Hsp70 might imply that ratoon cane was confronted with environmental stress in the soil, which possibly results from the presence of certain pathogens (pathogenic microbes or root-infecting nematodes) [44, 45] or other abiotic stresses in the ratooning system.

Hence, there are some interactions of protein-protein and protein

Hence, there are some interactions of protein-protein and protein-pore involved in the protein transition. Figure 4 Current blockage histograms as a function of applied voltage at medium voltages. The histograms of time duration are fitted by exponential distribution. An exponential function of dwell time versus voltage is defined in the inset. As mentioned above, the current blockage signals reveal the information of the size, conformation, Givinostat mouse and interactions of proteins passing through the nanopore. According to both t d and I b, different types of discrete current blockades are characterized

in Figure 5. For type I, the current signal has a typical spike shape with a deep intensity and a short dwell time. For type II, the current blockage turns to be rectangle with a similar amplitude but a long transition time. For type III, a distinct asymmetric and retarded current signal is observed with an even longer transition time. Usually, the negatively charged protein will flash past the nanopore driven by the strong electric force within the nanopore, giving the short-lived event as type I. However, given a protein with a high content of charged residues, a variety of electrostatic and hydrophobic interactions are involved in the liquid–solid interface PFT�� between the protein

and nanopore [31]. Once the protein is absorbed in the pore wall, the current signal will be blocked persistently, and it recovers till the protein is desorbed and impelled out the nanopore, showing as the long-lived events of types II and III. The type II event shows an abrupt restore, implying a very fast release of absorption. In contrast, the type III event shows a triangle-shaped signal and a longer restore period, implying a gradual release of absorption. Since the electric field (and thus the main driving force) within the nanopore is much stronger than that around the mouths of the nanopore (see Figure 2), it is reasonable to speculate that the absorption in the type II case is within the pore Suplatast tosilate while that

in type III is near the pore mouths. Owing to the decaying electric field in the pore mouth, there is a complicated equilibrium of adsorption and desorption involved between the protein and nanopore in type III. The absorption of protein to the nanopore wall also slows down the velocity of protein translocation, which accounts for the smaller diffusion constant D of proteins in the pore. In contrast with the prolonged dwell time from hundreds of milliseconds to several minutes obtained by small nanopores, the protein adsorption time is shortened and the frequency of the long-lived events is also find more decreased in larger nanopores. Especially, with the increase of the voltage, the adsorption phenomenon is gradually weakened by the enhanced driving force, and the velocity of protein transition is also speeded up.

This therapy is not only used in genetic deficiencies, but also i

This therapy is not only used in genetic deficiencies, but also in other complicated diseases, such as viral infection (human immunodeficiency virus), autoimmunity (rheumatoid arthritis), cancer, diabetes, coronary, and selleckchem artery disease [5]. With the progress of this technique, gene therapy will become an effective therapeutic method for neurodegenerative conditions, hemophilia, AIDS, asthma, and the myriad of other genetic and acquired

diseases that affect humanity [2]. By considering the mentioned issues, the choice of a suitable method for DNA delivery to the targeted cells beseems very important at the point of receiving appropriate genes. Although gene therapy can be carried out using naked DNA into the target cells, having negative nature of cellular membrane and negative charge of large DNA molecules, the nucleic acid-based therapeutics cannot cross cellular membranes by simple passive diffusion methods. Hence, to facilitate the transfer of DNA molecules into a cell, the existence of a vector is necessary [6, 7]. Viral and non-viral vectors, two major types of vectors for gene delivery, are currently being utilized in clinical trials at similar levels. In gene delivery,

it is relatively common to follow biomimetic approaches. Biological systems include modified viruses and mildness bacteria. Viral vectors are more efficient than non-viral vectors for

DNA delivery but may present a CB-839 ic50 significant risk to patients, selleck while non-viral carriers are inherently ifenprodil safer than viral carriers [8–10]. Furthermore, in contrast to the viral gene delivery systems, the non-viral carriers are expected to be less immunogenic, with simple preparation and a possible versatile surface modification [7]. The non-viral vectors are usually made of lipids or polymers with/without using other inorganic materials where they can also be prepared from a lipid-polymer or lipid-polymer-inorganic hybrid. The choice of gene delivery strategies among several delivery systems depend on some factors including the improvement of vectors, kind of expression systems, and better understanding of molecular biology of target site and employing of the advances in the identification of new genes and new targets [11]. Recently, nanotechnology approaches play an important role in the design novel and efficient non-viral gene delivery vectors. In this review, we will focus on introducing lately synthesized nanoparticles as vectors with gene delivery applications. Non-viral vectors In considering the viral gene delivery vector safety concerns regarding the risk of excessive immune response (adenovirus) and insertion mutagenesis (retroviruses), the use of non-viral vectors can overcome the mentioned safety problems [12].

All statistical analyses were performed by SPSS 17 0 software pac

All statistical analyses were performed by SPSS 17.0 software package for Windows. P<0.05 was regarded statistically significant. Results The mRNA expression of seven stem-cell-associated markers in biopsy samples obtained through bronchoscopy The expression of Bmi1, CD133, CD44, Sox2, Nanog, OCT4 and Msi2 mRNA in bronchoscopic biopsies of lung check details cancer and non-cancer patients are presented in Table 2 Aurora Kinase inhibitor and Figure 1. Overall, the mRNA expression of seven markers was higher in the malignant group than in the benign group. However, the mRNA relative levels of Bmi1, CD133 and CD44 by RT-PCR were not

significantly different between lung cancer and non-malignant lung tissues analyzed by Mann–Whitney U test, nor were the expression rates of CD44 and Msi2. We found that the Bmi1 positive expression rate was significantly correlated with histology types (P=0.007) and differentiation (P=0.027), while the positive rate of Nanog was negatively correlated with differentiation (0.032). However, the positive expression rates of CD133, CD44, Sox2, OCT4 and Msi2 did not correlate with age, gender, histological type, stage and differentiation of lung cancer (Table 3). Table 2 mRNA expression of stem cell makers in human lung cancer

and non-cancer Torin 2 concentration lung tissues   Lung cancer Non-cancer P Lung cancer Non-cancer P   Positive rate, %(n) Positive rate, %(n)   Expression, χ ± s Expression, χ ± s Value Bmi1 88.4(99/112) 66.7(12/18) 0.026 0.60±0.73 0.32±0.29 0.118 CD133 85.7(96/112) 55.6(10/18) 0.006 0.77±0.90 0.58±0.97 0.057 CD44 98.2(110/112) 88.9(16/18) 0.092 1.67±1.77 1.44±1.33 0.606 Sox2 98.2(110/112) 83.3(15/18) 0.019 2.06±2.15 0.99±1.53 0.001 Nanog 63.4(71/112) 33.3(6/18) 0.016 0.23±0.42 0.04±0.09 0.013 OCT4 85.7(96/112)

38.8(7/18) <0.0001 0.46±0.50 0.12±0.27 <0.0001 Msi2 96.4(108/112) 94.4(17/18) 0.531 1.29±1.13 0.47±0.51 <0.0001 Figure 1 Example RT-PCR bands of human lung cancer and non-lung cancer biopsy tissues obtained from bronchoscopy. Total RNAs were isolated and reverse transcribed to cDNA from the biopsy tissues. RT-PCR Products Digestive enzyme of β-actin and stem-cell-associated markers were run on 2% agarose gels with ethidium bromide. Table 3 Correlation between stem cell mRNA expression of biopsy samples and lung cancer clinical features   Analyzable Bmi1 expression P* CD133 expression P* CD44 expression P* Sox2 expression P* Nanog expression P* OCT4 expression P* MSi2 expression P*   cases Postive, n(%)   Postive, n(%)   Postive, n(%)   Postive, n(%)   Postive, n(%)   Postive, n(%)   Postive, n(%)   Age                               <60 57 51(89.5) 0.716 48(84.2) 0.643 56(98.2) 1 55(96.

Plain X-rays of the abdomen reveal dilatation of the small bowel

Plain X-rays of the abdomen reveal dilatation of the small bowel and air-fluid levels [3]. CT scan, eventually with oral contrast, shows the dilatation of proximal bowel and the collapse of distal bowel [4, 5]. Also ultrasounds may be AZD4547 useful [6, 7]. The key of management of small bowel obstruction is the identification of intestinal strangulation,

because mortality increases from 2 to 10 folds in such cases. Therefore an immediate surgical repair with an eventual bowel resection is mandatory. However, the clinical diagnosis of small bowel strangulation is extremely difficult and CT scan becomes very useful, usually on the basis of either bowel wall thickening, mesenteric edema, asymmetrical enhancement with contrast, pneumatosis, or portal venous gas. Mortality for small bowel obstruction has decreased during the past 50 to 60 years from 25% to 5% [8–20]. find more Initial therapy aims at correction of depletion of intravascular fluids and electrolyte

abnormalities. The patient should be given nothing by mouth and nasogastric tube should be inserted in patients with emesis. In patients with adhesive small intestine obstruction, water-soluble contrast medium (Gastrografin®) with a follow-through study has not only a diagnostic but also a therapeutic role, because it is safe and reduces the operative rate and the time to resolution of obstruction, as well as the hospital stay [21–23]. Surgical intervention is 3-Methyladenine cell line instead mandatory for patients with a complete small bowel obstruction with signs or symptoms indicative of strangulation, perforation or those patients with simple obstruction that has not resolved within 24 to 48 hours Amino acid of non operative treatment [23]. The surgical approach

includes adhesiolysis and resection of non viable intestine. The extension of intestinal resection depends on the purple or black discoloration of ischemic or necrotic bowel. Viable intestine also has mesenteric arterial pulsation and normal motility. When ischemic damage is more limited, is sufficient adhesiolysis followed by a 10-15 minutes period of observation to allow for possible improvement in the gross appearance of the involved segment. The role of laparoscopy in small bowel obstruction has still to be defined. Certainly, laparoscopy represents a diagnostic act and sometimes has a therapeutic role [24, 25]. The major indication is small bowel obstruction due to unique band adhesion without signs of ischemia and necrosis. In laparoscopic procedures the first trocar has to be positioned using Hasson’s technique for open laparoscopy to avoid accidental bowel perforations related to bowel distension and adhesions with the abdominal wall. After that, two 5 mm trocars must be introduced under vision to explore the peritoneal cavity and find the bowel segment obstructed by the band adhesion. If ischemic or necrotic bowel is present conversion to open surgery may be necessary.

This modification could also explain the increased resistance to

This modification could also explain the Z-DEVD-FMK mouse increased resistance to Az in F. tularensis LVS. In addition, there are methylases that can confer increased resistance by targeted

modification (methylation) of a specific adenine residue of the 23S rRNA. There are some methylases that have been identified as critical virulence factors for Francisella that might carry out this modification [39]. Some methylases that are present in the genome of F. novicida are either absent or are pseudogenes/nonfunctional genes (such as FTT0010, FTT0770, FTT1430, FTT1719, and FTT1735c) in F. tularensis Temsirolimus order Schu S4, potentially contributing to the different sensitivities to Az between the strains [34]. Any potential role of these molecules in Az sensitivity or resistance in Francisella has not yet been determined. It has been suggested that Az attaches to the acidic LPS on the outer membrane of gram-negative bacteria, allowing the drug to penetrate through the outer membrane and enter the bacteria [40]. The wbt locus in Francisella, which is responsible for the production of LPS O-antigen, has been shown to be required for virulence [41]. In published reports, the wbtA mutant mTOR inhibitor in F. tularensis LVS demonstrated a loss of the O-antigen and an inability to replicate in mouse macrophages. F. novicida wbtA mutants replicate normally and have only moderate sensitivity to serum [42, 43]. We tested F. novicida transposon-insertion mutants wbtN, wbtE, wbtQ

and wbtA, which are involved in the production of LPS, and found that these mutants were less susceptible to Az. Mutations of the LPS in the F. novicida transposon LPS O-antigen mutants may alter the LPS region presumed to bind to Az, resulting in a decreased amount of Az penetration and increased resistance to Az. Our results support the proposed role of LPS O-antigen in Az penetration into gram-negative bacteria such as Francisella. Az is a weak base that can remain inside host cells for a longer time at a higher concentration than in the serum.

This occurs because the basic amine groups of Az neutralize the lysosomal pH and prevent acidification of the lysosome. This process causes the drug to become trapped in the cell due to the positive charge. The drug is slowly released from polymorphonuclear neutrophils, allowing for a long half-life [8]. Az Exoribonuclease also concentrates in macrophages, which suggested to us that it might be useful as a potential treatment of intracellular pathogens such as F. tularensis. J774A.1 mouse macrophage were infected with F. philomiragia, F. novicida, and F. tularensis LVS and treated with Az. It was determined that 5 μg/ml Az was effective in eliminating intracellular F. philomiragia, F. novicida, and even F. tularensis LVS infections in J774A.1 cells. Although Type B strains are intrinsically more resistant to macrolides, F. tularensis LVS CFUs were eliminated below the Az MIC values for this strain. We suggest that J774A.

β-lactamase enzymes inactivate β-lactam antibiotics, by hydrolyzi

β-lactamase enzymes inactivate β-lactam antibiotics, by hydrolyzing their β-lactam ring essential to antibiotic

function [15, 16]. There is a wide array of βTrichostatin A -lactamases with varying specificities and activities, and this resistance Lazertinib mechanism has clinical significance [16–18]. Notably, many of the ‘ESKAPE’ pathogens (E nterococcus faecium, S taphylococcus aureus, K lebsiella pneumonia, A cinetobacter baumanni, P seudomonas aeruginosa and E nterobacter species), responsible for a majority of nosocomial infections [19], may produce β-lactamases. Alongside the ever-growing threat of Methicillin Resistant S. aureus (MRSA), Methicillin Susceptible S. aureus (MSSA) strains are also highly prevalent and responsible for severe infections such

as infective endocarditis [20, 21]. Both MRSA and MSSA can produce β-lactamases [22–25]. Though MK-8776 mw by historical definition, expression of an altered target penicillin binding protein PBP2’ with lowered affinity for β-lactam antibiotics results in methicillin resistance [26–28], β-lactamase alone may be responsible for borderline methicillin/oxacillin resistance phenotype even in strains without PBP2’ [29]. Most MRSA strains produce β-lactamase in addition to PBP2’ [22–24]. Among MSSA, ~90% strains are β-lactamase producers [30]. β-lactamases can therefore present a challenge to successful anti-bacterial therapy, in particular where the bacterial burden is high. Cephalosporins are the treatment of choice for MSSA infections [31–33]. Although traditionally cephalosporins were believed to be stable to the S. aureus β-lactamases, an ‘inoculum effect’ has been demonstrated, wherein at high inocula some cephalosporins get hydrolysed by β-lactamases [34, 35]. The inoculum effect with different cephalosporins has been reported in

clinical isolates of MSSA [33, 36], and instances of clinical failure of cephalosporins are well documented in high-inoculum staphylococcal endocarditis infections and bacteremia [37–40]. The inoculum Avelestat (AZD9668) effect is not limited to Staphylococcus, and is observed in other bacteria including Enterobacteriaceae, Pseudomonas and Neisseria gonorrhoeae, with antibiotic classes other than cephalosporins as well [35]. Evaluation of antibiotic susceptibility and detection of resistance are mainly performed by means of disk diffusion assays or broth/agar dilution to determine minimum inhibitory concentration (MIC = lowest concentration of antibiotic that inhibits the bacterial growth), where bacteria are cultured in the presence of antimicrobials and respective growth patterns observed [41, 42]. Besides agar or broth dilution, the E-test is a relatively new, yet established method for MIC determination, and consists of a predefined gradient of antibiotic concentrations on a plastic strip (http://​www.​biomerieux-diagnostics.​com).

Prog Polym Sci 2000, 25:1503–1555 CrossRef 8 Van Beilen JB, Poir

Prog Polym Sci 2000, 25:1503–1555.CrossRef 8. Van Beilen JB, Poirier Y: Production of renewable polymers from crop plants. Plant J 2008, 54:684–701.PubMedCrossRef 9. Budde CF, Riedel SL, Willis LB, Rha C, Sinskey AJ: Production of poly(3-hydroxybutyrate-

co -3-hydroxyhexanoate) from plant oil by engineered Ralstonia eutropha strains. Appl Environ Microbiol 2011, 77:2847–2854.PubMedCrossRef 10. Fukui T, Suzuki M, Tsuge T, Nakamura S: Microbial synthesis of poly(( R )-3-hydroxybutyrate- co -3-hydroxypropionate) from unrelated carbon sources by engineered Cupriavidus necator . Biomacromolecules 2009, 10:700–706.PubMedCrossRef 11. Kawashima Y, Cheng W, Mifune J, Orita LY2603618 cell line I, Nakamura S, Fukui T: Characterization and functional analyses of R -specific enoyl Coenzyme A hydratases in polyhydroxyalkanoate-producing Ralstonia eutropha . Appl Environ Microbiol 2012, 78:493–502.PubMedCrossRef 12. Matsusaki H, Abe H, Taguchi K, Fukui T, Doi Y: Biosynthesis of poly(3-hydroxybutyrate- co AZD0156 concentration -3-hydroxyalkanoates) by recombinant bacteria expressing the PHA synthase gene phaC1 from Pseudomonas sp. 61–3. Appl

Microbiol Biotechnol 2000, 53:401–409.PubMedCrossRef 13. Mifune J, Nakamura S, Fukui T: Targeted engineering of Cupriavidus necator chromosome for biosynthesis of poly (3-hydroxybutyrate- co -3-hydroxyhexanoate) from vegetable oil. Can J Chem 2008, 86:621–627.CrossRef 14. Mifune J, Nakamura S, Fukui T: Engineering of pha operon on Cupriavidus necator chromosome for Apoptosis Compound Library manufacturer efficient biosynthesis of poly(3-hydroxybutyrate- co -3-hydroxyhexanoate) from vegetable oil. Polym Degrad Stab 2010, 95:1305–1312.CrossRef

15. Tsuge T, Yano K, Imazu S, Numata K, Kikkawa Y, Abe H, Taguchi S, Doi Y: Biosynthesis of polyhydroxyalkanoate (PHA) copolymer from fructose using wild-type and laboratory-evolved PHA synthases. Macromol Biosci 2005, 5:112–117.PubMedCrossRef 16. Pohlmann A, Fricke WF, Reinecke F, Kusian B, Liesegang H, Cramm R, Eitinger T, Ewering C, Pötter M, Schwartz E, Strittmatter A, Voss I, Gottschalk G, Steinbüchel A, Friedrich B, Bowien B: Genome sequence of the bioplastic-producing “Knallgas” bacterium Ralstonia eutropha H16. Nat Biotechnol 2006, 24:1257–1262.PubMedCrossRef 17. Peplinski K, Ehrenreich A, Döring C, Bömeke M, Reinecke F, Hutmacher C, Steinbüchel Sucrase A: Genome-wide transcriptome analyses of the “Knallgas” bacterium Ralstonia eutropha H16 with regard to polyhydroxyalkanoate metabolism. Microbiology 2010, 156:2136–2152.PubMedCrossRef 18. Brigham CJ, Budde CF, Holder JW, Zeng Q, Mahan AE, Rha C, Sinskey AJ: Elucidation of β-oxidation pathways in Ralstonia eutropha H16 by examination of global gene expression. J Bacteriol 2010, 192:5454–5464.PubMedCrossRef 19. Marioni JC, Mason CE, Mane SM, Stephens M, Gilad Y: RNA-seq: an assessment of technical reproducibility and comparison with gene expression arrays. Genome Res 2008, 18:1509–1517.PubMedCrossRef 20.