The reduced pain level lasted up to 9 months after the third treatment [17]. It is unclear how fast and in what amount the small dosage of lignocaine diffuses through the peritoneum and reaches the blood after pertubation. In the above clinical study, serum samples were

therefore collected before and after the treatment for later analysis of lignocaine in serum. This observational study reports the serum concentration of lignocaine after pertubation of 10 mg lignocaine hydrochloride. The hypothesis is that the pertubated dosage of 10 mg lignocaine hydrochloride reaches the central circulation and gives rise to low systemic levels of lignocaine. 2 Methods 2.1 Study Design, Participants and Procedures A randomized, double-blind and controlled study was conducted www.selleckchem.com/products/azd1390.html to study VE 822 the effect of pertubation with lignocaine (1 mg/ml, 10 ml) on dysmenorrhoea and quality of life. A total of 42 patients were included in the study, 24 of whom were randomized to active treatment and 18 to placebo. The methods of this trial have previously been described in detail [17]. The patients were recruited through advertisements and from the gynaecological outpatient unit at the three participating clinics in Stockholm, Sweden. The first patient was included in March 2007 and the last in November

2008. The main inclusion criteria were presence of peritoneal or ovarian endometriosis buy Gefitinib verified by laparoscopy and dysmenorrhoea, with a pain score of >50 mm on the visual analogue scale (VAS). The exclusion criteria included reduced patency in the fallopian tubes and the intention to achieve pregnancy during the forthcoming year. Detailed eligibility criteria for the study have been previously published [17]. Written informed SN-38 datasheet consent was obtained before any study-related procedures, and the CONSORT (Consolidated Standards of Reporting Trials) guidelines were followed. The procedure was approved by the Medical Products Agency in Sweden, 8

November 2006 (151:2006/56028) and after amendment, 12 December 2007 (151:2007/76934), as well as by the Regional Ethical Review Board in Stockholm, 10 January 2007 (2006/1416-32) and after amendment, 14 December 2007 (2007/1398-32). Before inclusion, the patients were scrutinized and tested concerning all criteria. Three treatments were given pre-ovulatory on cycle day 6–12 in three sequential menstrual cycles, since the effect on dysmenorrhoea increased after repeated treatments [7]. A thin plastic catheter (PBN-Medicals, Stenløse, Denmark) was inserted and cuffed in the cervical canal or in the caudal part of the uterine cavity; 10 ml of ringer-lignocaine 1 mg/ml (active treatment) or ringer acetate (placebo) was infused through the uterine cavity and pertubated into the peritoneal cavity.

Figure 4 Qualitative UV assay and mRNA analysis of E. coli R391 mutants KOA, KOB and KOC. (A) AB1157 R391 mutants KOA, KOB and KOC. UV254nm exposure increasing (12 J.m-2) from left to right. (i) From top to bottom, AB1157, AB1157 R391, AB1157 R391 KOA. (ii) AB1157, AB1157 R391 KOB. (iii) AB1157, AB1157 EPZ015666 ic50 R391, AB1157 R391 KOC. (B) SYBR® Safe stained 1% (w/v) agarose gel confirming orf43 mRNA transcription in AB1157

R391 KOA. M, Bioline Hyperladder I DNA marker; 1, AB1157 R391 RNA negative control; 2, AB1157 R391 genomic DNA positive control; 3, AB1157 orf43 cDNA; 4, AB1157 R391 orf43 cDNA; 5, KOA orf43 cDNA; 6, KOB orf43 cDNA; 7, KOC orf43 cDNA; 8, KOB orf20 cDNA. Primers used specific to orf43 generated a 188 bp PCR product. Primers SB525334 supplier used for lane 8 only were specific for the kanamycin resistance gene of ICE R391, orf20, which generated a PCR product of 223 bp. Amplification of orf20 specific cDNA was carried out to show KOB and KOC RNA was not degraded. Lane 1 negative control was DNase treated RNA that was not converted to cDNA. (C) Map of exact locations of KOA, KOB and KOC deletions on ICE R391 genome. The KOA,

KOB and KOC ampicillin resistance cassettes and associated promoter were inserted into the ICE R391 genome in the reverse complement to prevent the ampicillin resistance cassette promoter inducing the transcription of orf43 mRNA. The KOA deletion removed all possible promoters of orf43 in front of the gene and left the last 36 bp specific to the preceding orf42 gene. The KOB deletion removed the

same region as KOA and the 36 bp region. The KOC deletion was a duplicate of KOA with an additional Vildagliptin zeocin resistant orfs90/91 deletion. Site-directed mutagenesis of Orf43 Bioinformatic analysis of orf43 indicated that it belongs to a highly conserved TraV-like family of transfer proteins involved in type IV secretion systems required for conjugation [8]. Site-directed mutagenesis of pBAD33-orf43 was carried out to convert two leucines at a.a. positions 47 and 48 to prolines in the predicted Orf43 protein (GenBank: AAM08037). Insertion of two prolines was expected to disrupt the α-helical transmembrane spanning region of Orf43 by creating a 30° bend [19]. This mutation was found to cause loss of the cytotoxic function of pBAD33-orf43[8] as there was no observable decline in host cell growth rates after induction of the mutant clone compared to the wild type clone [Figure 5A,B]. Since introduction of membrane disruptive mutations abolish the effect, this is suggestive that membrane association is required in addition to over-expression of the Orf43 protein for sensitisation and Cell Cycle inhibitor cytotoxicity associated with this ICE product.

Thus, BED values are calculated by clicking on the button “”BED and Fractionaction Calculation”". Figure 4 Example of IsoBED LY3009104 solubility dmso calculation for the case of prostate and lymph nodes treatment. Then the SIB schedule is calculated by selecting the control

box “”IsoBED Calculation”". The results of such evaluations are visualized in the “”IsoBED DOSES”" area. The dose limits are visualized in the “”OAR CONSTRAINTS”" area. DVH import Import procedures consist of copying DVH files, exported from TPS, in a folder with the patient’s name contained in a directory where an IsoBED.exe file is installed. DVH files are different depending on the TPS source. IsoBED can import DHV data files from Eclipse, Pinnacle and Brainscan. Dose distribution and radiobiological analysis RG7112 concentration Figures 5, 6 and 7 show different screens generated by the software through which different types of evaluations for prostate-pelvis, head & neck and lung cases can be performed. On the right side of the screen there is a window where the

patient of interest can be selected, while in the lower part of the screen the fraction number, dose per fraction and the district of interest can be set. Thus, the total dose can be calculated and all the imported DVHs are visualized. Figure 5 DVHs imported from TPSs for Sequential and SIB Technique in a) prostate, b) Head & Neck and c) Lung cases. Numered circles represents the OAR costraints. Figure 6 NTD 2 -VH for Sequential

and SIB Technique in a) prostate, b) Head & Neck and c) Lung cases. Numered circles represents the OAR costraints. Figure 7 www.selleckchem.com/products/dinaciclib-sch727965.html Radiobiological curves (TCP, NTCP and P + ) for Sequential and SIB Technique in a) prostate, b) Head & Neck and c) Lung cases. Figures 5a, 5b and 5c show the DVHs imported from TPSs calculated with different modalities (SIB and sequential). The user can choose which volume of interest to view by selecting them from a list visualized at the lower-left corner of the screen. Furthermore, in the same area, the total volume or one between, the minimum, maximum, average, median and modal dose percentage for each plan and each structure shown in the Sitaxentan histogram is displayed. In order to perform radiobiological calculations the (α/β)values can be set for each structure by choosing a dropdown menu in which the list of parameters incorporated in a dedicated database appears. These values are derived from literature data and from experience at our Institute [9–20]. The “”NTD2″” button transforms every DVH into the NTD2VH (Figures 6a, 6b and 6c). Finally, the TCP, NTCP and P+ curves against the dose prescribed to the reference target can be calculated with the “”TCP-NTCP”" button and their values are shown in the lower area of the screen (Figures 7a, 7b and 7c). Software Validation All the outcomes from IsoBED software were compared with an automatic excel spreadsheet specially designed for this purpose.

Biochim Biophys Acta 2011, 1814:29–35.PubMedCrossRef 37. Lamb DC, Maspahy S, Kelly DE, Manning NJ, Geber A, Bennett JE, Kelly SL: Purification, reconstitution, and AMN-107 mouse inhibition of cytochrome P-450 sterol Δ22-desaturase from the pathogenic fungus Candida glabrata. Antimicrob Agents Chemother 1999, 43:1725–1728.PubMed

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Cifuentes V: Differential carotenoid production and gene expression in Xanthophyllomyces dendrorhous grown in a nonfermentable carbon source. FEMS Yeast Res 2011, 11:252–262.PubMedCrossRef 45. Lodato P, Alcaíno J, Barahona S, Niklitschek M, Carmona M, Wozniak A, Baeza M, Jiménez A, Cifuentes V: Expression of the carotenoid biosynthesis genes in Xanthophyllomyces dendrorhous. Biol Res 2007, 40:73–84.PubMedCrossRef 46. Miao L, Chi S, Tang Y, Su Z, Yin T, Guan G, Li Y: Astaxanthin biosynthesis is enhanced Methane monooxygenase by high carotenogenic gene expression and decrease of fatty acids and ergosterol in a Phaffia rhodozyma mutant strain. FEMS Yeast Res 2011, 11:192–201.PubMedCrossRef 47. Calo P, Miguel T, Velázquez JB, Villa TG: Mevalonic acid increases trans-astaxanthin and carotenoid biosynthesis in Phaffia rhodozyma. Biotechnol Lett 1995, 17:575–578.CrossRef 48. Shimada H, Kondo K, Fraser PD, Miura Y, Saito T, Misawa N: Increased carotenoid production by the food yeast Candida utilis through metabolic engineering of the isoprenoid pathway. Appl Environ Microbiol 1998, 64:2676–2680.PubMed 49. Parks LW, Casey WM: Physiological implications of sterol biosynthesis in yeast. Annu Rev Microbiol 1995, 49:95–116.PubMedCrossRef 50.

equorum Chicken 3 I ND 16 32 >64 >128 4 4 ERY, TET TYTJC8 S. equorum Chicken 3 I ND 16 32 64 64 16 2 OXA, CIP, GEN, ERY TDPJC13 S. sciuri Chicken 1 E P 64 64 >64 >128 32 4 OXA, CIP, GEN, TET TDPJC5 S. sciuri Chicken 1 R ND 32 >64 >64 >128 >64 16 OXA, GEN, ERY, TET TLKJC2 S. sciuri Chicken 6 Q P 16 >64 >64 >128 16 8 OXA, CIP, GEN, ERY, TET TDP12 S. simulans Pork 1 A ND >64 64 64 64 16 4 OXA, CIP, GEN, ERY, RIF TDP24 S. simulans Pork 1 B ND 32 >64 >64 64 2 4 TET THTJC2 S. simulans Chicken 5 O P 64 32 >64 >128 4 4 OXA, CIP, GEN, ERY, RIF TLD12 S. simulans Pork 2 K P >64 >64 >64 >128 64 8 OXA, CIP, GEN, ERY,

RIF, TET TLD20 S. simulans Pork 2 M P >64 >64 >64 128 32 4 OXA, CIP, GEN, ERY, RIF, TET TLD22 S. simulans Pork

2 G2 P 16 >64 >64 128 8 8 CIP, GEN, ERY, TET TYT6 S. simulans Pork 3 G1 ND 16 >64 >64 >128 64 4 OXA, ERY, TET Recipient RN4220 S. aureus         4 4 0.25 0.5 0.25 1 ND RN4220-pHNLKJC2 S. aureus         32 64 16 16 8 4 ND DH5α E. coli         4 ABT-263 clinical trial 4 – - – - ND DH5α-pUC18-cfr E. coli         8 8 – - – - ND ATCC 29213 S. aureus         2 2 0.12 0.5 0.06 1   aPatterns that differed JPH203 from pattern A by six or more bands were considered to represent different strains. Patterns that differed by fewer than six bands were considered to represent subtypes within the main group (e.g.,L1, L2). bP, plasmid; ND, not determined. cCHL, chloramphenicol; FFC, florfenicol; CLR, clindamycin; TIA, tiamulin; VAL, valnemulin; LZD, linezolid. MIC was not measured because of known intrinsic resistance or naturally

high MICs. dThe results were interpreted according to Eucast breakpoints ( http://​www.​eucast.​org/​clinical_​breakpoints/​). OXA, oxacillin; CIP, ciprofloxacin; GEN, gentamycin; ERY, erythromycin; RIF, rifamycin; TET, tetracycline. All isolates were susceptible to vancomycin. ND, not determined. Results of Southern blotting indicated that 14 isolates harbored cfr in their plasmid DNA (Table  1). The remaining eight isolates appeared to carry cfr in their genomic DNA; however, this assumption needs to be further BIRB 796 cell line confirmed by S1-PFGE. unless Only one cfr-carrying plasmid (designated as pHNLKJC2) that originated from a chicken isolate, TLKJC2, was transformed into Staphylococcus aureus RN4220. The transformant was confirmed by polymerase chain reaction (PCR) for cfr; it showed the same PFGE pattern as that of Staphylococcus aureus RN4220. Antimicrobial susceptibility of cfr-positive Staphylococcus isolates and the transformants All of the 22 cfr-positive staphylococcal isolates had elevated minimum inhibitory concentrations (MICs) against chloramphenicol (16 to > 64 mg/L), florfenicol (32 to >64 mg/L), clindamycin (≥64 mg/L), tiamulin (64 to > 128 mg/L), valnemulin (0.5 to >64 mg/L), and linezolid (2 to 16 mg/L) (Table  1). In addition, 18, 14, 13, 17, 6, and 17 isolates exhibited resistance to oxacillin, ciprofloxacin, gentamicin, erythromycin, rifampicin, and tetracycline, respectively.

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5. Harman T, Taylor P, Walsh M, La Forge B: Quantum dot superlattice thermoelectric materials and devices. Science 2002,297(5590):2229–2232.CrossRef 6. Yang JM, Yang H, Lin LW: Quantum dot nano thermometers reveal heterogeneous local thermogenesis in living cells. ACS Nano 2011,5(6):5067–5071.CrossRef 7. Chen KH, Chien CY, Li PW: Precise Ge quantum dot placement for quantum tunneling devices. Nanotechnology 2010, 21:055302.CrossRef 8. Chen KH, Chien CY, Lai WT, George T, Scherer A, Li PW: Controlled heterogeneous nucleation and growth of germanium quantum dots on nano-patterned silicon dioxide and silicon nitride substrates. J Crystal Growth & Design 2011, 11:3222.CrossRef 9. Chien CY, Chang YJ, Chen KH, HDAC phosphorylation Lai WT, George T, Scherer A, Li PW: Nanoscale, catalytically-enhanced local HSP990 datasheet Oxidation of silicon-containing layers by ‘burrowing’ Ge quantum dots. Nanotechnology 2011, 22:435602.CrossRef 10. Kuo MH, Wang CC, Lai WT, George T, Li

PW: Designer Ge quantum dots on Si: a heterostructure configuration with enhanced optoelectronic performance. Appl Phys Lett 2012,101(11):223107.CrossRef 11. Chang JE, Liao PH, Chien CY, Hsu JC, Hung MT, Lee SW, Chen WY, Hsu TM, George T, Li PW: Matrix and quantum confinement effects on optical and thermal selleck chemicals properties of Ge quantum dots. J Phys D: Appl Phys 2012,45(10):15303–15308.CrossRef 12. Ostwald W: Lehrbuch der Allgemeinen Chemie, vol. 2, part 1. Leipzig: Engelmann; 1896. 13. Ratke L, Voorhees PW: Growth and Coarsening:

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Total RNA was extracted and reverse transcribed into cDNA, which was then used for amplification of CDK8 and

β-catenin. The real time PCR conditions consisted of 1 cycle at 94°C for 10 min followed by 40 cycles at 94°C for 30 s, at 55°C for 30 s, and at 72°C for 30 s. GAPDH was employed as an internal standard. The primer sequences were as Fludarabine follows: 5′-GAGCGGGTCGAGGACCTGTTTGAAT-3′ (forward) and 5′-ACATGCCGACATAGAGATCCCAGTTCCTTC-3′ (reverse) for CDK8; 5′-TGCCAAGTGGGTGGTATAGAG-3′ (forward) and 5′-TGGGATGGTGGGTGTAAGAG-3′ (reverse) for β-catenin; 5′AGGGGCCATCCACAGTCTTC3′ (forward) and 5′ AGAAGGCTGGGGCTCATTTG 3 (reverse) for GAPDH. The 2 -ΔΔCT method was applied to analyze the relative changes in click here gene expression. Western blot analysis As described previously [14], following 72 h of transfection, total protein was extracted from HCT116 cells and subjected to SDS-PAGE. Protein concentrations were transferred onto PVDF membrane, then membranes were blocked and incubated with rabbit anti-human CDK8 (1:1000) or β-catenin antibody (1:1000) https://www.selleckchem.com/products/Thiazovivin.html at 4°C overnight. After 3 washes with TBS-T solution for 10 min, the membranes underwent hybridization with a goat anti-rabbit IgG secondary antibody (1:1000) at 37°C for 1 h. After

further washing, CDK8 and β-catenin levels were visualized using an ECL chemiluminescence kit. Immunohistochemistry The protein expression of CDK8 and β-catenin

in 47 tumor tissues and adjacent normal tissues were detected by IHC. Samples were fixed in 10% neutral formaldehyde, embedded in paraffin, and sliced. Briefly, the paraffin-embedded tissues were serially cut into 4 μm sections, dewaxed, and rehydrated. Sections were then Reverse transcriptase blocked with peroxide and non-immune animal serum and incubated sequentially with rat anti-human CDK8 and β-catenin (1:1000), and biotin-labeled goat anti-rabbit IgG (1:1000). Finally, the sections were stained with DBA, counterstained with hematoxylin, dehydrated, cleared in xylene, and fixed. Histological assessment was performed as described previously [15]. Immunostaining was independently examined by two clinical pathologists who were unaware of the patient outcome. Five high-power fields (400 × magnification) were randomly counted for each section. The brown staining on the cytoplasm was read as positive reactivity for CDK8 and β-catenin. The presence of brown colored granules on the cytoplasm was taken as a positive signal, and was divided by color intensity into not colored, light yellow, brown, tan and is recorded as 0, 1, 2, 3, respectively. We also choose five high-power fields from each slice and score them. Positive cell rate of < 25% was a score of 1, positive cell rate of 25~50% was a score of 2, positive cell rate of 51~75% was a score of 3, positive cell rate of > 75% was a score of 4.

Acad Emerg Med 1998, 5:951–960.PubMedCrossRef 21. Bignardi T, Burnet S, Alhamdan D, et al.: Management of women referred to an acute gynecology unit: impact of an ultrasound-based model of care. Ultrasound Obstet Gynecol 2010, 35:344–348.PubMedCrossRef 22. Toret-Labeeuw F, Huchon C, Popowski T, Chantry A, Dumont A, Fauconnier A: Routine ultrasound examination by OB/GYN residents increase the accuracy of diagnosis for emergency surgery in gynecology. World J Emerg Surg 2013,8(1):16.PubMedCentralPubMedCrossRef 23. Moll HA: Challenges 3-Methyladenine in vivo in the validation of triage systems at emergency departments. J Clin Epidemiol 2010, 63:384–388.PubMedCrossRef 24. Rouzier R, Coutant C, Lesieur

SB-715992 B, et al.: Direct comparison of logistic regression and recursive partitioning to predict chemotherapy

response of breast cancer based on clinical pathological variables. Breast Cancer Res Treat 2009, 117:325–331.PubMedCrossRef 25. Shariat SF, Karakiewicz PI, Suardi N, Kattan MW: Comparison of nomograms with other methods for predicting outcomes in prostate cancer: a critical analysis of the literature. Clin Cancer Res 2008, 14:4400–4407.PubMedCrossRef 26. Abbott J: Pelvic pain: lesson from anatomy and physiology. J Emerg Med 1990, 8:441–447.PubMedCrossRef 27. Lamvu G, Steege JF: The anatomy and neurophysiology of pelvic pain. J Minim Invasive Gynecol 2006, 13:516–522.PubMedCrossRef 28. Houry D, Abbott JT: Ovarian torsion: a fifteen-year review. Ann Emerg Med click here 2001, 38:156–159.PubMedCrossRef 29. Milholland AV, Wheeler SG, Heieck JJ: Medical assessment by a Delphi group opinion technic. N Engl J Med 1973, 288:1272–1275.PubMedCrossRef Competing interest The authors declare that they have no competing interests. Authors’ contributions CH and AF wrote the manuscript. AF, AD and BF designed the study. AAC, CH and AF collected the datas. CH, AD and AF performed the statistical analysis.”
“Diagnosis and treatment of perforated peptic ulcer (Dr. S. Di Saverio MD) Introduction Every year peptic ulcer disease (PUD) affects 4

PFT�� in vivo milion people around the world [1]. Complications are encountered in 10%-20% of these patients and 2%-14% of the ulcers will perforate [2, 3]. Perforated peptic ulcer (PPU) is relatively rare, but life-threatening with the mortality varying from 10% to 40% [2, 4–6]. More than half of the cases are female and they are usually older and have more comorbidities than their male counterparts [6]. Main etiologic factors include use of non-steroidal anti-inflammatory drugs (NSAIDs), steroids, smoking, Helicobacter pylori and a diet high in salt [3, 7]. All these factors have in common that they affect acid secretion in the gastric mucosa. Defining the exact etiological factor in any given patient may often be difficult, as more than one risk factor may be present and they tend to interact [8].

In addition see more 9 non-cancerous gallbladders and 9 non-cancerous bile duct controls were obtained from patients who had resections for diseases not involving the gallbladder or bile duct (in these patients

the gallbladder or bile duct was removed for surgical access to other hepatobiliary or pancreatic structures). Each DZNeP nmr sample was re-examined histologically using H&E-stained cryostat sections. Surrounding non-neoplastic tissue was dissected from the frozen block under 10× magnification and care was taken that at least 90% for remaining cells were cancerous. All studies were approved by the Memorial Sloan-Kettering IRB. RNA isolation, probe preparation, and expression microarray hybridization Total RNA was isolated from tissue using the DNA/RNA all prep kit (Qiagen, Germantown, Maryland, USA).

Quality of RNA was ensured before labeling by analyzing 20–50 ng of each sample using the RNA 6000 NanoAssay and a Bioanalyzer 2100 (Agilent, Santa Clara, California, USA). Samples with a 28S/18S ribosomal peak ratio of 1.8–2.0 and a RIN number >7.0 were considered suitable for labeling. RNA from one IHC specimen, two EHC specimens, and three cases of GBC failed to meet this standard and were discarded from the gene expression analysis. For the remaining samples, 2 μg of total RNA was used for cDNA synthesis using an oligo-dT-T7 primer and the SuperScript Double-Stranded cDNA Synthesis Kit (Invitrogen, Carlsbad, California, USA). Synthesis, linear amplification, AZD5582 mw and labeling of cRNA were accomplished by in-vitro transcription using the MessageAmp aRNA Kit (Ambion, Austin, Texas, USA) and biotinylated nucleotides (Enzo Diagnostics, New York, USA). Ten

micrograms of labeled and fragmented cRNA were then hybridized to the Human HG-U133A GeneChip (Affymetrix, Santa Clara, California, USA) at 45°C MRIP for 16 hours. Post hybridization staining, washing were processed according to manufacturer. Finally, chips were scanned with a high-numerical aperture and flying objective lens in the GS3000 scanner (Affymetrix). The image was quantified using GeneChip Operating Software (GCOS) 1.4 (Affymetrix). Array CGH profiling Genomic DNA was extracted using the DNA/RNA prep kit (Qiagen). DNA integrity was checked on a 1% agarose gel and was intact in all specimens except one case of EHC. 3 μg of DNA was then digested and labeled by random priming using RadPrime (Invitrogen) and Cy3 or Cy5-dUTP. Labeled DNA was hybridized to 244 K CGH arrays (Agilent) for 40 hours at 60°C. Slides were scanned and images quantified using Feature Extraction 9.1 (Agilent). Real-Time PCR 1 ug of total RNA was reverse-transcribed using the Thermoscript RT-PCR system (Invitrogen) at 52°C for 1 h.

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2005:397–415. 33. Patek M, Nesvera J, Guyonvarch A, Reyes O, Leblon G: Promoters of Corynebacterium glutamicum . J Biotechnol 2003, 104:311–323.PubMedCrossRef 34. Peters-Wendisch PG, Stansen KC, Götker S, Wendisch VF: Biotin protein ligase from Corynebacterium glutamicum : role for growth and L-lysine production. Appl Microbiol Biotechnol

2011, in press. 35. Rodionov DA, Mironov AA, Gelfand MS: Conservation of the biotin regulon and the BirA regulatory signal in Eubacteria and Archaea. Genome Res 2002, 12:1507–1516.PubMedCrossRef 36. Rodionov DA, Gelfand MS: Computational identification of BioR, a transcriptional regulator of biotin metabolism in Alphaproteobacteria Vitamin B12 , and of its binding signal. FEMS Microbiol Lett 2006, 255:102–107.PubMedCrossRef 37. Rodionov DA: Comparative genomic reconstruction of transcriptional regulatory networks in bacteria. Chem Rev 2007, 107:3467–3497.PubMedCrossRef 38. Eitinger T, Rodionov DA, Grote M, Schneider E: Canonical and ECF-type ATP-binding cassette importers in prokaryotes: diversity in modular organization and cellular functions. FEMS Microbiol Rev 2011, 35:3–67.PubMedCrossRef 39. Finkenwirth F, Neubauer O, Gunzenhauser J, Schoknecht J, Scolari S, Stockl M, Korte T, Herrmann A, Eitinger T: Subunit composition of an energy-coupling-factor-type biotin transporter analysed in living bacteria. Biochem J 2010, 431:373–380.PubMed 40. Ko YT, Chipley JR: Role of biotin in the production of lysine by Brevibacterium lactofermentum . Microbios 1984, 40:161–171.PubMed 41. Peters-Wendisch PG, Schiel B, Wendisch VF, Katsoulidis E, Mockel B, Sahm H, Eikmanns BJ: Pyruvate carboxylase is a major bottleneck for glutamate and lysine production by Corynebacterium glutamicum . J Mol Microbiol Biotechnol 2001, 3:295–300.PubMed 42.