J Trauma 1999, 47:896–902. discussion 902–893.PubMedCrossRef 23. Heyde CE, Ertel W, Kayser R: [Management of spine injuries in polytraumatized patients]. Orthopade 2005, 34:889–905.PubMedCrossRef 24. Blauth M, Knop C, Bastian L, Krettek C, Lange U: [Complex injuries of the spine]. Orthopade 1998, 27:17–31.PubMed 25. Woltmann A, Buhren V: [Shock trauma room management of spinal injuries in the framework of multiple trauma. A systematic Poziotinib mw review of the literature]. Unfallchirurg 2004, 107:911–918.PubMedCrossRef 26. Buhren V: [Injuries to the E1 Activating inhibitor thoracic and lumbar spine]. Unfallchirurg 2003, 106:55–68. quiz 68–59.PubMedCrossRef 27. Welkerling H, Wening JV, Langendorff

HU, Jungbluth KH: [Computer-assisted data analysis of injuries of the skeletal system in polytrauma patients]. Zentralbl Chir 1991, 116:1263–1272.PubMed 28. McLain p38 MAPK signaling pathway RF, Benson DR: Urgent surgical stabilization of spinal fractures in polytrauma patients. Spine 1999, 24:1646–1654.PubMedCrossRef

29. Richter-Turtur M: [Spinal injuries in polytrauma patients]. Langenbecks Arch Chir Suppl Kongressbd 1992, 311–315. 30. Kossmann T, Trease L, Freedman I, Malham G: Damage control surgery for spine trauma. Injury 2004, 35:661–670.PubMedCrossRef 31. Patel RV, DeLong W Jr, Vresilovic EJ: Evaluation and treatment of spinal injuries in the patient with polytrauma. Clin Orthop Relat Res 2004, 43–54. 32. Prasad VS, Schwartz A, Bhutani R, Sharkey PW, Schwartz ML: Characteristics of injuries to the cervical spine and spinal cord in polytrauma patient population: experience from a regional trauma unit. Spinal Cord 1999, 37:560–568.PubMedCrossRef 33. Buhren V: [Fractures and instability buy Depsipeptide of the cervical spine]. Unfallchirurg 2002, 105:1049–1066.PubMedCrossRef 34. Morris

CG, McCoy E: Clearing the cervical spine in unconscious polytrauma victims, balancing risks and effective screening. Anaesthesia 2004, 59:464–482.PubMedCrossRef 35. Morris CG, Mullan B: Clearing the cervical spine after polytrauma: implementing unified management for unconscious victims in the intensive care unit. Anaesthesia 2004, 59:755–761.PubMedCrossRef 36. Stahel PF, Heyde CE, Wyrwich W, Ertel W: [Current concepts of polytrauma management: from ATLS to ""damage control""]. Orthopade 2005, 34:823–836.PubMedCrossRef 37. Haas NP, Hoffmann RF, Mauch C, von Fournier C, Sudkamp NP: The management of polytraumatized patients in Germany. Clin Orthop Relat Res 1995, 25–35. 38. Ruchholtz S, Zintl B, Nast-Kolb D, Waydhas C, Lewan U, Kanz KG, Schwender D, Pfeifer KJ, Schweiberer L: Improvement in the therapy of multiply injured patients by introduction of clinical management guidelines. Injury 1998, 29:115–129.PubMedCrossRef 39. Committee ACoS: Advanced Trauma Life Support (ATLS) for Doctors, Chicago/IL. 7th edition. 2004. 40. Jarrar D, Chaudry IH, Wang P: Organ dysfunction following hemorrhage and sepsis: mechanisms and therapeutic approaches (Review).

Analyzing the O-antigen gene clusters of 8 sequenced strains (Lai, Fiocruz BMS-907351 research buy L1-130, JB197, L550, Gui44, Lin4, Lin6, and C401), we developed simple and practical PCR assays for six epidemic serogroups in China [32] that target serogroup-specific

genes and employed to identify strains isolated from clinical samples. Results and Discussion MAT All strains, including 75 reference strains and 40 isolated strains, were tested by MAT with standard rabbit serum. The results are shown in additional file 1 Table S1 and additional file 2 Table S2. The serology results for all reference strains are consistent with those of the National Institute for the Control of Pharmaceutical and Biological Products. Of the 40 isolated strains, 7 strains belong to serogroup Icterohaemorrhagiae,, 5 strains belong to serogroup Autumnalis, 11 strains belong selleck compound to serogroup Grippotyphosa, 1 strain belongs to serogroup Hebdomadis and 5 strains belong to serogroup Sejroe. 5 isolated strains were validated by MAT as Serogroup Ballum, Australis, Javanica and Sarmin, respectively. Six strains were unable to be classified. None of strains belong to serogroup Canicola Development of PCR-Based Assays We assigned functions of all ORFs by comparing homology genes. Most of predicted proteins are shown to be related SB431542 ic50 to O-antigen

biosynthesis except for some hypothetical proteins (see additional file 3 Table S3-6). For typing bacteria, several different approaches have been used in Leptospira. Serological typing is based on strain to strain differences in the structure

of lipopolysaccharide, mainly in the structure of the O-antigen. Recently, PCR-based typing methods targeting specific genes were employed for dicrimination certain serogroups of several bacteria [14–17]. These targeted genes are mainly those encoding glycosyltransferase and enzymes involved in O-antigen assembly. Among them, two highly specific genes: wzx (encode O-unit flippase) and wzy (encode O-antigen polymerase), are O-genotyping targets, usually. Previous analysis of the O-antigen of Leptospira showed that the biosynthesis of LPS in Leptospira Cediranib (AZD2171) is a Wzy-dependent pathway [12, 33]. In conjunction with published data [34], our comparison of the O-antigen clusters in all 8 strains shows that the Wzy protein has a high identity among the different serogroups. Similarly, Wzx shows high similarity across other serogroups (data not shown). So we discarded these two genes as PCR assays targets. To identify highly specific genes for PCR typing, we analyzed all predicted ORFs by the BLAST program. First, we selected genes that exhibit less than 70% amino acid similarity with their counterpart genes. Second, we compared these selected genes with draft data generated by 454 sequencing and discarded genes with more than 70% nucleotide similarity to any sequence in the draft data.

Consequently, more effective nutritional strategies need to be discovered. In the present study, the effects of EPZ5676 BCAA supplementation combined with taurine on a highly intense ECC-induced DOMS and muscle damage were investigated via a randomized, placebo-controlled, and double-blind trial, because taurine was reported to decrease oxidative stress induced by ECC [16]. In ECC-induced DOMS and muscle damage, subjective and objective parameters including VAS scores, CIR, and serum levels of LDH and 8-OHdG were significantly improved by the combination of

BCAA and taurine supplementation. This combined supplementation also tended to improve serum CK and aldolase activities, but not significantly. These parameters, especially serum CK activity, have a high degree of individual biological variability, and it is difficult to demonstrate a statistically significant difference between the small number of subjects [3]. Overall, the present study demonstrated that combined supplementation with BCAA and taurine is beneficial for see more reducing ECC-induced DOMS and muscle damage. However, it was impossible to determine whether the combined effects were due to the

synergistic effect of both BCAA and taurine or the sum of the individual effects. Compared with the effectiveness of BCAA supplementation on exercise-induced muscle soreness and damage reported in previous studies [4, 7, 9, 22, 25], BCAA supplementation alone was not sufficient to effectively inhibit muscle soreness and damage in the present study. This discrepancy might be due to differences in the exercise protocol (intensity and type) and the supplemental regimen (duration and dose). In a previous study by Shimomura et al., the authors recognized that the intensity was low in a squatting exercise where subjects used only their body weight because the changes in the levels of serum muscle damage markers, including CK and myoglobin, were very small over the three days following exercise [7, 8]. On the other hand, repeated arm extensions with

weight loads of 90% MVC in the present study caused a significant increase in serum muscle damage markers in the placebo group, thereby implying higher exercise intensity. Glutathione peroxidase The present findings with this higher intensity suggest that a combination of BCAA and taurine taken EVP4593 order during high-intensity exercise may prevent severe muscle soreness and damage that cannot be attenuated by BCAA alone. In addition to exercise intensity, the amount of oral BCAA intake is one of the important factors for preventing exercise-induced muscle soreness and damage. Shimomura et al. suggested that the BCAA dose should be adjusted according to body mass to at least 92–100 mg/kg because the inhibitive effects of BCAA on DOMS and muscle damage were greater in females than in males [7, 8]. The BCAA dose in the present study should be sufficient because daily BCAA supplementation at 9.6 g/day worked out to 145.67 ± 5.3 mg/kg.

Sometimes oral NSAIDs drugs are restrictedly applied mainly for the reason to stimulate patient’s gastric mucosa. Intravenous flurbiprofen axetil injection could avoid this side effect. In all of 1089 cases, the side effect incidence rate was very low about 2.9% [18]. Most side effects were in gastrointestinal tract such as nausea, vomit, diarrhoea or in neuropsychosis such as fever, fear cold, Trichostatin A sleepiness, etc. Few cases expressed as subcutaneous bleeding or pain in the injecting site. Perhaps our cases were insufficient,

no side effect of flurbiprofen axetil was found in this study. Conclusion In general, cancer pain is considered as chronic. The pain intensity ranges from mild to severe and present for a long time. Harmless approach to therapy such as by oral or by cutaneous are suggested by WHO. But, for some reasons as constipation and psychosomatic symptoms, there has many patients whose can not take drugs by oral, or can not be used cutaneous anaesthetic drugs, intravenous flurbiprofen axetil could exactly remedy the anaesthetic drug’s shortcoming, and let itself to be an important switch drug. Acknowledgements The authors thank other staffs working in the department of medical oncology,

the first affiliated hospital of Anhui medical university for they supported our work. References 1. Villars P, Dodd M, West C, Koetters T, Paul SM, Schumacher K, Tripathy D, Koo selleck chemicals P, Miaskowski C: Differences in the prevalence and severity of side effects based on type of analgesic prescription in patients with chronic cancer pain. J Pain Symptom Manage 2007, 33: 67–77.CrossRefPubMed 2. Fallon M, McConnell S: The principles of cancer pain management. Clin Med 2006, 6: 136–139.PubMed aminophylline 3. Roszkowski MT, Swift JQ, Hargreaves KM: Effect of NSAID administration on tissue levels of immunoreactive prostaglandin E2, leukotriene B4, and (S)-flurbiprofen Screening Library following extraction of impacted third molars. Pain 1997, 73:

339–345.CrossRefPubMed 4. Karasawa F, Ehata T, Okuda T, Satoh T: Propofol injection pain is not alleviated by pretreatment with flurbiprofen axetil, a prodrug of a nonsteroidal anti-inflammatory drug. J Anesth 2000, 14: 135–137.CrossRefPubMed 5. Yamashita K, Fukusaki M, Ando Y, Fujinaga A, Tanabe T, Terao Y, Sumikawa K: Preoperative administration of intravenous flurbiprofen axetil reduces postoperative pain for spinal fusion surgery. J Anesth 2006, 20: 92–95.CrossRefPubMed 6. Mizuno J, Sugimoto S, Kaneko A, Tsutsui T, Tsutsui T, Zushi N, Machida K: Convulsion following the combination of single preoperative oral administration of enoxacine and single postoperative intravenous administration of flurbiprofen axetil. Masui 2001, 50: 425–428.PubMed 7.

By doing so, we found that ALS1, ALS2 and ALS5 were overexpressed in all model systems, but their fold upregulations were more pronounced in both in vitro models and in the in vivo model, compared to the RHE model.

Using mutant strains, it was already demonstrated that Als1p and Als2p are involved in biofilm formation on abiotic surfaces [29, 34]. Furthermore, ALS4 was highly upregulated in the two in vitro models, and was extremely overexpressed in the RHE and in vivo models. However, deletion of ALS4 did not significantly reduce biofilm formation on silicone and neither resulted in reduced biomass on RHE, but it is likely that Als2p compensates for the loss of ALS4 [34]. Our data clearly show high expression levels for ALS4 in biofilms grown on mucosal surfaces as well as on abiotic surfaces in vitro and in vivo, suggesting see more a role for Als4p in C. albicans Stattic in vitro biofilms. For ALS6 and ALS9, on the other hand, model-dependent up- and downregulations were observed. ALS6 was not overexpressed in the RHE model, which is not surprising as Als6p reduces adhesion of the fungus to buccal epithelial cells [35]. In both in vitro models and in the in vivo model, on the other hand, we observed an upregulation of ALS6. Using RT-PCR, it was previously shown that ALS6 was weakly expressed in biofilms grown on silicone [21]. However, using real-time PCR, we detected low Ct values (i.e. high

absolute mRNA levels) for ALS6 (data not shown). Furthermore, ALS9 is downregulated in the RHE model, in the MTP and in the vivo model, whereas this

gene is slightly upregulated under flow conditions in the CDC reactor. It is possible that shear stress generated in the CDC reactor induces the expression of ALS9, although further research is needed to confirm this hypothesis. We also studied the expression of ALS3 and HWP1, two genes that encode hyphae-specific adhesins [36, 37]. Their expression levels were higher in the CDC reactor than in the MTP, and the percentage of Vactosertib manufacturer filaments was also higher in biofilms grown in the CDC reactor. Hyphae are known for their increased adhesive properties [13], and presumably shear stress in the CDC reactor triggers the fungus to form more filaments, which Y-27632 mw in turn express more ALS3 and HWP1. We also found that the percentage of filaments gradually decreased during biofilm formation in both in vitro models. It is known that contact-sensing induces filamentation in C. albicans [38], and therefore it is likely that initial contact of the fungus with the silicone results in filamentation. This could explain why young biofilms contain more filaments than mature ones in both in vitro models. Furthermore, ALS3 and HWP1 were highly upregulated in biofilms grown in the RHE model, and we found an increase in the percentage of filaments during biofilm formation in this model system. In order to grow in the RHE model, C.

The PCR product was cloned as a HindIII fragment into pRK7813 and the resultant construct was named pMA157. This construct was Selleck Androgen Receptor Antagonist introduced

into Rm11430 by triparental conjugation using MT616 as the mobilizer strain. Growth Phenotype of Rm11430 and ability to survive long-term carbon starvation Mutants of phaC, phaB, and bdhA all demonstrate impaired growth on PHB cycle intermediates [23, 24]. To determine if a lesion in phaZ resulted in a similar impairment in Tubastatin A the capacity of S. meliloti to utilize PHB Cycle intermediates, the growth of Rm11430 was compared to that of Rm1021, Rm11105 [23], Rm11107 [23] and Rm11347 [24] on TY, YMA, and minimal media containing either 15 mM acetate (A), acetoacetate (AA) or D-3-hydroxybutyrate (HB) as sole carbon sources. No difference in growth phenotype was observed between Rm11430 and Rm1021 (Table 1). Table 1 Growth Phenotypes of S. meliloti PHB Cycle Mutants Strain Relevant Characteristics YMA Phenotype Carbon Source Utilization       Glucose

D-3-HB Acetate AA Rm1021 wild-type Mucoid + + + + Rm11105 phaC::Tn5 Dry + – + – Rm11107 bdhA::Tn5 Mucoid + – + + Rm11347 phaBΩ Dry + – + – Rm11430 phaZΩSmSp Mucoid + + + Selleck CX-6258 + The ability of the phaZ mutant strain to withstand long-term carbon starvation was tested, relative to both Rm1021 and Rm11105, by incubation for 4 weeks in M9 liquid medium with no added carbon source. Cells were grown to late-log in YMB and washed twice in M9. A 1:50 dilution was used to inoculate 75 ml of M9 salts. Starting cfu/ml was determined immediately following inoculation by serial dilution of a 1 ml aliquot. Starting cultures

typically contained approximately 2 × 105 cfu/ml. These starting values were each given a relative value of 1. 1 ml samples were removed at 7 day intervals and serial dilutions were used to determine cfu/ml. Values presented are the averages of 3 independent cultures. The data in Figure. 1 show that the ability to synthesize and/or break down PHB has a significant impact on long-term survival in the absence of an exogenous carbon source. The wild-type strain Rm1021 is capable of increasing cell density during the early stages of starvation, presumably by degrading readily mobilizable intracellular carbon stores, a pattern Decitabine mw which is not seen in either the phaZ or phaC mutants. Figure 1 Viable cell counts of S. meliloti PHB mutants following incubation in minimal media with no exogenous carbon source added. Values presented are the average of three independent cultures. Rm1021 cells are able to maintain viability for almost 4 weeks following transition to a carbon-free environment. In contrast, both Rm11105 and Rm11430 demonstrate a significant decrease in viability under the same conditions. PHB accumulation To assess the effect of the phaZ lesion on PHB content in Rm11430, total PHB accumulation of stationary-phase cells was measured and compared to the wild-type strain Rm1021.

On the contrary, PMM1390 (hli10) was

slightly transcribed (Sheet 3 of Additional file 3). It may that differentially expressed hli genes protect different cellular components, such as light harvesting antenna and nucleic acids [45, 49]. As expected, phage-related genes displayed the lowest FHPI research buy expression levels in this study, check details as phage infection conditions were not tested. It would be better to have phage infection condition data to analysis these genes expression profiles. For phosphorus and nitrogen acquisition genes, there was no significant enrichment in the four expression subclasses (Figure 5b). However, PMM1119 and PMM112 (two P-limitation-inducible porins) [47], and one ammonium transporter (amt1, PMM0263) were highly expressed (Sheet 3 of Additional file 3), suggesting AZD5363 ic50 that these proteins play particular roles

in phosphorus or nitrogen uptake, respectively. Conserved genes more likely clustered to operon than poorly conserved genes We identified 210 operons (49.8% of total) that uniquely belonged to the core genome, whereas the flexible genome harbored only 86 operons (20.4% of total). Based on this observation, we examined whether operon genes were more conserved than non-operon genes. The comparison of nonsynonymous substitution rates indicated that the total operon coding-sequence genes indeed evolve more slowly than non-operon genes (P < 0.001; Figure 6a). Furthermore, operon genes were significantly overrepresented in the core genome but not in the flexible

genome (Figure 6b). Because HEG are more conserved in MED4, we compared the operon rate (the ratio of operon genes to total genes in a certain gene collection) of HEG with the other expression subclasses. We found that operons are strikingly enriched in HEG and MEG (Figure 6b). In addition, the distribution of operon size within the core genome when compared with the flexible genome was slightly different. Approximately 63.8% (134/210) of operons detected in the core genome harbored two genes, compared with 72.1% (62/86) in the flexible genome (P = 0.065). Extensive works has reported that essential genes prefer to be in operon [50, 51]. We compared the operon rate of DEG-hit genes and DEG-miss genes. Significantly more operonic genes were indeed present in the former gene set (62.7% > 57.6%; P = 0.042). Sclareol These findings strongly suggest that MED4 conserved genes are more likely to be co-transcribed and are larger in size. Figure 6 Operon distribution of different expression subclasses. (a) Comparison of nonsynonymous substitution rate between operon genes and non-operon genes in MED4 (Mann–Whitney U Test, two-tailed). A circle represents an outlier. (b) Operon rate of four expression subclasses (HEG, MEG, LEG, and VEG) or the core/flexible genomes (Fisher’s exact test, one-tailed). The operon rate was defined as the ratio of operon genes to total genes in a certain gene collection. The operon rate of each subclass was normalized by the whole genome operon rate (55.5%). P-value ≤ 0.

The results of this analysis are given in Tables 3 and 4. Also, additional file 5 contains the organisms comprising each random group, as well as the core EVP4593 proteome size and unique proteome size of each. Table 3 Results of protein content cohesiveness experiments     Core proteomes Unique proteomes S N I P C P U Bacillus anthracis 3 4941 2123 ** 0/25 168 1 ** 0/25 Bacillus cereus 4 2881 1840 ** 0/25 2 0 – 0/25 Bacillus thuringiensis

2 4255 2864 ** 5/25 4 7 n.s. 7/25 Brucella abortus 3 2699 2603 ** 6/25 2 1 * 4/25 Brucella suis 2 3025 2760 ** 2/24 5 4 n.s. PRI-724 mw 5/24 Burkholderia ambifaria 2 5609 3798 ** 1/25 198 17 ** 0/25 Burkholderia cenocepacia 3 5908 3352 ** 0/25 168 0 ** 0/25 Burkholderia

mallei 4 3623 3086 ** 1/25 18 0 – 0/25 Burkholderia pseudomallei 4 4972 3086 ** 0/25 45 0 – 0/25 Clostridium botulinum 8 1514 763 ** 0/25 10 0 – 0/25 Clostridium perfringens 3 2110 1085 ** 0/25 298 0 ** 0/25 Lactobacillus casei 2 2355 959 ** 0/25 593 5 ** 0/25 Lactobacillus delbrueckii 2 1372 959 ** 0/25 222 5 ** 0/25 Lactobacillus reuteri 2 1402 959 ** 0/25 120 5 ** 0/25 Mycobacterium bovis 2 3822 2577 ** 1/25 36 38 n.s. 3/25 Mycobacterium tuberculosis 3 3724 2118 ** 0/25 26 17 n.s. 3/25 Neisseria gonorrhoeae 2 1795 1560 ** 0/8 229 3 ** 0/8 Neisseria meningitidis 4 1547 1426 ** 0/14 75 4 ** 0/14 mTOR inhibitor Column headings are: S, species; N I , number of sequenced isolates of species S; , core proteome size of the sequenced isolates of S; , average core proteome size of the randomly-generated sets; P C , probability that the average core proteome size of the randomly-generated sets is different MycoClean Mycoplasma Removal Kit than the core proteome size of the sequenced isolates of S; , fraction of random sets having a core proteome larger than S. , , P U and are analogous to , , P C , and , respectively, and refer to the comparisons involving the number of proteins found in all sequenced isolates of S, but no other isolates

from the same genus (“”unique proteomes”"). In some cases, all of the random sets corresponding to a particular species had zero unique proteins. No P-value could be computed for these because the standard deviation of these values was zero. In these situations, the P U column contains a dash character (-). The averages in both column and column are rounded to the nearest whole number. For certain rows, column shows a value of 0; in some cases, this value is exact, while in other situations, it is due to rounding. If due to rounding, then the standard deviation of the random sets is non-zero, and column P U contains a P-value. For columns P C and P U , “”n.s.”" means “”not significant”", a single asterisk indicates a P-value of less than 0.05, and a double asterisk indicates a P-value of less than 0.001. See Table 4 for the continuation of this table.

find more Figure 3 TEM images and SAED patterns of α-Fe 2 O 3 hexagonal plates (a, b), α-Fe 2 O 3 hexagonal bipyramid (c, d), and Fe 3 O 4 polyhedral particles (e, f). To further understand the formation process of Fe3O4, the reaction

systems with the addition of both KOH and EDA were hydrothermally synthesized at 200°C for different reaction times, as shown in Figure 4. Figure 4a shows that, after 2 h of growth, the main phase of the particles is α-Fe2O3 hexagonal plates. The edge of the hexagonal SGC-CBP30 mw plate is not as straight as that obtained for the reaction system with KOH only. As the reaction time increased to 5 h, as shown in Figure 4b, small octahedron particles were observed and the original hexagonal plate started to dissolve and no longer maintained the hexagonal shape. As the reaction time continued to increase to 7 h, more polyhedron particles were observed with larger sizes and only a small amount of plate-like

particles still existed, as shown in Figure 4c. At the reaction time of 9 h, the observed particles are mainly polyhedron ones, as shown in Figure 4d. The first observation in this sequence of experiment is that KOH can rapidly transform iron hydroxides to hematite. The second observed phenomenon is that the α-Fe2O3 hexagonal plates were dissolved to become irregular plates during the transformation process. Figure 4 Mixture of α-Fe 2 O 3 and Fe 3 O 4 particles precipitated in the hydrothermal system at 200 °C at different times. (a) 2 h, (b) 5 h, (c) 7 h, and (d) 9 h. The result implied that phase transformation Selleckchem Cilengitide evolved in four steps: (1) the reaction systems rapidly transformed Fe(OH)3 or FeOOH to α-Fe2O3 hexagonal plates under the hydrothermal conditions, (2) the α-Fe2O3 hexagonal plates dissolved gradually, (3) the reduction process causes valence transition of Fe3+ to Fe2+, and (4) the Fe3O4 particles started to nucleate and then finally grew to form polyhedral particles. To further understand Y-27632 cell line the role of NO3 – ions on the phase

transition process, the precursor of FeNO3 was substituted by FeCl3 with the same hydrothermal conditions. Two cases were investigated, one with the addition of KOH only and the other with the addition of both KOH and EDA under the same hydrothermal condition of 200°C for 9 h. Figure 5a shows that the α-Fe2O3 hexagonal plates were obtained when the reaction system consists of FeCl3 and KOH, while the phase transformation from α-Fe2O3 hexagonal plates to Fe3O4 polyhedral particles still occurred when the reaction system consists of FeCl3, KOH, and EDA, as shown in Figure 5b. The shape of the polyhedral particles is more irregular in this case. The XRD patterns, shown in Figure 4c, confirmed the related phases. Notice that the α-Fe2O3 plates were not completely reduced to Fe3O4 particles. Thus, NO3 – ions are not directly involved in the reduction process of Fe3+ to Fe2+.

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