) column (150 mm × 2.1 mm, i.d. 5 μm). The mobile phase comprised A = methanol/water with 5 mM ammonium formate (20 : 80) and B = methanol/water

with 5 mM ammonium formate (90 : 20); the gradient programme was: 0–1 min 98% A, 1–8 min 98–5% A, 8–12 min 5% A, 12–13 min 5–98% A and 13–20 min 98% A phases. The column oven temperature was set at 35 °C with a flow rate of 0.4 mL min−1. An aliquot of 10 μL was injected through an auto sampler. Mass spectrometric analysis was performed with electrospray ionization (ESI) in positive (5500 eV) modes for each sample. The nebulizer gas and heater gases were adjusted at 30 and 55 p.s.i., respectively. The ion source temperature was set BIBW2992 ic50 at 500 °C. A hybrid triple quadrupole linear ion trap mass spectrometer (QqQLIT) was used by integrating an EMS-triggered IDA-enhanced production (EPI), resulting in enhanced sensitivity at trace level. IDA-EPI

experiments were automatically triggered to obtain product ion mass spectra of these peaks. In the IDA experiment, the parameters included rolling collision energy with scan speed of 4000 amus−1, and dynamic trap Selleck Palbociclib fill time as a dependent scan. Chlorimuron-ethyl (50 mg) was dissolved in distilled water (100 mL). The pH of the solution was adjusted to 2.5 by the addition of concentrated sulfuric acid (2 mL). The solution was stirred magnetically for 48 h at 42 °C and then kept for 4 days at room temperature. Products formed were separated by preparative thin-layer chromatography, purified by crystallization from benzene and characterized by spectroscopic methods. The compounds were 4-methoxy-6-chloro-2-amino pyrimidine (III) [IR (cm−1): 3460, 3323, 802; 1H-NMR (CDCl3) δ: 6.2 (s, 1H, aromatic), Galactosylceramidase 5.3 (s, 2H, NH2), 3.85 (s, 3H, OCH3); mass spectrum: 159 (M+, 27.7%, 129 (M+ - 30), 94 (M+-66,12.6%) and ethyl-2-(aminosulfonyl)benzoate (IV) [IR (cm−1): 3382, 3278, 2367, 1723; 1H-NMR (CDCl3) δ: 8.15 (d, 1H, aromatic, J = 7 Hz), 7.85 (d, 1H, aromatic, J = 5 Hz), 7.65 (t, 2H, aromatic, J = 5 Hz), 5.84 (s, 2H, NH2), 4.46 (q, 2H, OCH2CH3, J = 5 Hz), 1.46 (t, 3H, OCH2CH3, J = 7 Hz);

mass spectrum: 229 (M+, 8.5%), 212 (10.6%), 184 (100%) and 121]. Fungi isolated from rice rhizosphere soil were allowed to grow in minimal media with chlorimuron-ethyl as the carbon and nitrogen source. Only one fungus survived and grew in medium with chlorimuron as high as 200 mg L−1 (Fig. 1). The mycelia of the isolated fungus were nonseptate with a foot-cell, and conidiophores ended in a terminal enlarged ellipsoidal spherical swelling. This spherical vesicle bearded phialides that covered its entire surface and therefore the head of the conidia was mop-like. They were highly branched; multinucleate mycelia bore a large number of conidiophores, which arose individually as hyphae. Chains of conidia arose on the sterigma, giving the appearance of strings of beads. This fungus was characterized as A. niger.

β-Galactosidase activity due to the core 16S/23S rRNA gene promoter in Sulfolobus was 1.7–3-fold lower in the stationary phase than in exponential growth (Fig. 3). The pattern of β-galactosidase activity did not change significantly when normalized for

the absolute copy number of the lacS gene by qPCR, indicating that the increase in activity in exponential growth selleck chemical was due to regulation of the 16S/23S rRNA gene promoter, not gene dosage (Fig. 3b). The 42-bp 16S/23S rRNA gene core promoter is the smallest reported regulated promoter for Sulfolobus. These findings are consistent with evidence of upregulation of rRNA transcription during exponential growth in E. coli and Saccharomyces cerevisiae (yeast) (Nomura, 1999) and with microarray data from halophilic archaea showing that ribosomal protein gene transcription is higher during exponential growth than in the stationary phase (Lange et al., 2007). Moreover, rRNA in crude preparations from Natronococcus occultus decreases in the stationary phase (Nercessian

& Conde, 2006). The mechanism for core rRNA promoter regulation in S. solfataricus is obscure. The decrease in β-galactosidase activity observed during the stationary phase may be due to growth rate-dependent transcriptional regulation or stringent control in response to decreasing nutrient availability and/or charged tRNAs. The latter has been ABT-263 order shown to decrease total stable RNA accumulation in Sulfolobus (Cellini et al., 2004). As in E. coli and yeast, it is likely that there are multiple mechanisms contributing to regulation of the Sulfolobus 16S/23S rRNA gene operon. There is considerable

evidence that archaeal transcriptional regulators interact with core promoters, either binding between or overlapping the TATA box and the transcriptional start site (Peng et al., 2011). In vivo and in vitro analyses have determined several regulatory regions and the start site of the 16S/23S rRNA gene in S. shibatae selleckchem (Hudepohl et al., 1990; Reiter et al., 1990; Hain et al., 1992; Qureshi et al., 1997). The core promoter sequences necessary for transcription initiation in vitro are between −38 and −2 bases relative to the transcription start, identical to those used here in vivo. This region encompasses the proximal promoter element (PPE) (an AT-rich sequence −11 to −2 conserved in Sulfolobus stable RNA promoters), the TATA box, and several bases upstream thereof (Reiter et al., 1990), later identified as a transcription factor B (TFB) recognition element (BRE) (Qureshi & Jackson, 1998). A weak positive regulatory region between −354 and −190 and a negative regulatory region between −93 and −38 were also found (Reiter et al., 1990).

The factors included in the fishbone diagram were brainstormed by the members of the team and were based on individual experience. The factors were not quantified. Of these reasons, the team specifically focused on ‘provider factors’ because among physicians there may be low awareness of venous thromboembolism evidence-based guidelines.[2] Several published studies have proposed multifaceted strategies

to change physician prescribing behaviour including education and incorporating the task into the physician’s workflow.[3, 4] Based on these strategies, the team brainstormed various interventions that could influence these ‘provider factors’ (Table 1). Create poster reminder to perform a DVT risk assessment. Conduct an in-service MI-503 solubility dmso regarding the importance of DVT prophylaxis Selleckchem BIBW2992 Nurse driven risk stratification and prophylaxis order Pharmacist

driven risk stratification and prophylaxis order Force function for DVT score and orders in the electronic medical record Computerized physician order entry Computerized DVT prophylaxis reminders The GIM team felt that the best intervention would be to embed the DVT risk-assessment tool and DVT orders into a standardized physician admission order-set and to educate users regarding the availability of the order-set. Users were not informed that the order-set was created to improve DVT prophylaxis rates. The team then created an aim statement that stated: ‘This this website project will increase the percentage of newly admitted GIM patients receiving optimal

DVT prophylaxis by developing a standardized medicine admission order-set with an embedded risk-assessment tool and DVT prophylaxis orders. The preliminary review indicated that there were 65 admitted GIM patients in a 1-month period. Of the 65 patient charts, VTE forms were completed by a physician in only two charts (3%). Of the 65 patients admitted, only 49 (75%) received appropriate prophylaxis. Two-month post-intervention data indicated that of 72 GIM patients audited in a 1-month period, the standardized admission orders were used 86% of the time and that 91% of the patients received optimal DVT prophylaxis. The number of patients receiving correct DVT prophylaxis increased from 75% to 91%. Chart review 1 year after the implementation of the order-set revealed that the increase in DVT prophylaxis was sustained at 95% even after the project was complete. Utilization of the embedded risk-assessment tool for DVT prophylaxis increased from 3% to 86% but declined to 64% at the 1-year review (Figure 2). However, the use of the DVT orders within the order-set remained high at 90%. Of the 72 patient charts audited at 2 months, patients were more likely to receive prophylaxis (94%) when the standardized order-set was completed versus when the orders were not completed (70%).

“
“To gain an insight into the chemotactic factors involved in chemotaxis, we exposed a virulent strain of Flavobacterium columnare to various treatments, followed by analysis of its chemotactic activity. The chemotactic activity of F. columnare was significantly (P<0.05) inhibited when cells were pretreated by sodium metaperiodate, and a major portion of the capsular layer surrounding the cells was removed. Pretreatment of F. columnare with d-mannose, d-glucose and N-acteyl-d-glucosamine significantly (P<0.05) inhibited its chemotaxis activity, whereas pretreatment of cells with d-fructose, l-fucose, d-glucosamine, d-galactosamine, d-sucrose and N-acetyl-d-galactosamine

selleck chemicals llc failed to inhibit its chemotactic activity. These results indicate that at least three carbohydrate-binding receptors (d-mannose, d-glucose and N-acteyl-d-glucosamine) associated

with the capsule of F. columnare might be involved in the chemotactic responses. The relative transcriptional levels of three gliding motility genes (gldB, gldC, gldH) of F. columnare compared Selleckchem JQ1 with 16S rRNA gene following the exposure of F. columnare to catfish skin mucus were evaluated by quantitative PCR (qPCR). qPCR results revealed that the transcriptional level of gldH was significantly (P<0.001) upregulated in normal F. columnare at 5 min postexposure to the catfish mucus. However, when F. columnare were pretreated with d-mannose, there was no upregulation of gliding motility genes. Taken together, click here our results suggest that carbohydrate-binding receptors play important roles in the chemotactic response to catfish mucus. Flavobacterium columnare, the causative agent of columnaris disease, is responsible

for significant economic losses in freshwater fish aquaculture worldwide. Many species of wild, cultured and ornamental fish are susceptible to columnaris disease (Austin & Austin, 1999). Channel catfish are especially susceptible to columnaris, with high mortality rates (Wagner et al., 2002). Columnaris disease is characterized by necrotic skin, fin and gill lesions containing yellow-pigmented bacteria aggregated in hay stack-shaped films (Austin & Austin, 1999). Flavobacterium columnare is a motile bacterium that moves by gliding motility over surfaces (McBride, 2001). It is considered to be a rapid glider (Youderian, 1998). Flavobacterium johnsoniae, a closely related species, is reported to glide at speeds up to 10 μm s−1 (Pate & Chang, 1979; Lapidus & Berg, 1982), and its gliding motion appears to require the recognition of extracellular components of the host by components of the bacterial cells to send signals to trigger the movement. Gliding motility of F. johnsoniae requires the expression of six genes: gldA, gldB, gldD, gldF, gldG and gldH (McBride et al., 2003), and it has been suggested that the mechanisms of gliding motility in F.

29 [95% confidence interval (CI) 0.92–1.80]. Rebound risks increased with decreasing levels of coverage: patients with 80–95% adherence had a 2.69% risk of rebound

(compared with 100% adherence: RR=1.62; 95% CI 1.23–2.14), patients with 60–80% adherence had a 3.15% risk of rebound (RR=1.90; 95% CI 1.39–2.61) and patients with adherence below 60% had a 3.26% risk of rebound (RR=1.97; 95% CI 1.40–2.78). When the percentage of drug coverage was analysed as a continuous variable (thus assuming that the true underlying relationship between adherence and the log risk ratio is linear) the risk of viral rebound decreased by 9% (RR=0.91; 95% CI 0.87–0.95; P=0.0001) per 10% higher coverage. After adjusting for potential confounding factors (variables shown in Table 2), low levels of drug coverage continued to be significantly associated with viral rebound: rates of viral rebound were increased by 51% (RR=1.51; 95% CI 1.14–1.99), EX 527 supplier 70% (RR=1.70; 95% CI 1.24–2.33) and 75% (RR=1.75;

95% CI 1.24–2.47) in patients who had drug coverage of 80–95, 60–80 and <60%, respectively (Fig. 2). When the drug coverage was analysed as a continuous variable, the risk of viral rebound decreased by 7% per 10% higher adherence (RR=0.93; 95% CI 0.88–0.98; P=0.004). Other Smad inhibitor independent predictors of viral rebound were shorter duration of VL suppression, higher number of previous virological failures, currently being on an unboosted PI regimen compared with an NNRTI-containing regimen, having experienced two or more treatment interruptions (while VL detectable at the time), having started HAART in the calendar period 1997–1999 compared with 2003–2006, and having a time-zero for the DCVL episode in the period 2002–2003 compared with 2006–2007. The results of the analysis stratified by most common current regimen (unboosted PI, boosted PI and NNRTI-based regimen) suggested that the risk of viral rebound at a particular level of adherence differed according to the regimen type received (Fig. 3). For example, at the lowest levels of adherence (≤60%), the risk of rebound was,

respectively, 5.24, 3.50 and 2.19%, for patients receiving unboosted until PI, boosted PI and NNRTI-based regimens, while among subjects who adhered completely these risks were 1.46, 1.89 and 1.47%, respectively. In sensitivity analyses, we considered the proportion of days covered by a prescription for at least one drug, instead of three, as our adherence measure and obtained similar results (data not shown). In addition, we considered the effect of modifying the definition of viral rebound from a threshold of 200 to 50 copies/mL. In this case, the overall risk of rebound was higher (5.36%) but the factors associated with rebound were generally similar. The estimated RR of VL rebound for a 10% higher coverage was 0.95 (95% CI 0.92–0.99), and after adjusting for the risk factors considered in the main analysis, the RR weakened marginally to 0.97 (95% CI 0.93–1.

Design.  The colour of enamel was recorded (normal, white, yellow or brown) in specific areas for ten extracted first permanent molars with MIH defects and ten extracted sound teeth. Laser fluorescence (LF) and

mineral density (MD) were measured for the same areas. A mixed model, using sample/tooth as a random effect, was used to estimate the relationship between the MD and the colour-coding, and between the MD and LF readings. Results.  The between-samples correlation coefficient for the colour coding and the MD was 0.99 (P < 0.001), and 0.83 (P < 0.001) for the LF and MD. Conclusions.  The degree of staining of MIH enamel, click here as assessed visually or by LF, may be used clinically to reflect the severity of the defect. “
“International Journal of Paediatric Dentistry check details 2011;

21: 422–431 Background.  The genotypic diversity of both Streptococcus mutans and Streptococcus sobrinus in children with different caries experience remains unclear. Aim.  To investigate the genotypic diversity of S. mutans and S. sobrinus in children with severe early childhood caries (SECC) and in caries-free (CF) children. Methods.  Stimulated saliva of 87 SECC and 91 CF children aged 3–4 years was collected and submitted to cultivation, and MS colonies were enumerated. The genomic fingerprint analysis of S. mutans and S. sobrinus was carried out using AP-PCR. Results.  One to five genotypes of S. mutans were colonized in an oral cavity of SECC and CF children; 85.5% Inositol oxygenase SECC children and 57.9% CF children harboured more than one genotype of S. mutans. One to three genotypes of S. sobrinus were detected from each SECC child; 31.25% SECC children harboured more than one genotype of S. sobrinus. And one genotype was colonized in each CF child. S. mutans isolates from different individuals displayed distinctive DNA fingerprints. Conclusions.  DNA fingerprints of S. mutans and S. sobrinus isolates from 3- to 4-year-old children displayed genetic polymorphism, and S. mutans has greater genetic diversity than S. sobrinus. SECC children harboured more genotypes of S. mutans and S. sobrinus

than CF children. “
“International Journal of Paediatric Dentistry 2011; 21: 23–28 Aim.  To investigate the prevalence and distribution of developmental enamel defects in children with cerebral palsy (CP) in Beijing, China. Design.  A total of 135 children aged 1.5–6 years with moderate or severe congenital CP diagnosed in Beijing Boai Hospital from year 2005 to 2009 were recruited. The children underwent dental examination at the hospital dental clinic. Results.  Enamel defects (opacity and/or hypoplasia) were found in 44 (32.6%) out of 135 CP children. Enamel hypoplasia was found in 35 (25.9%) of the CP children, opacity alone was found in 5 (3.7%) of the CP children, and mixed defects (opacity and hypoplasia) was found in 4 (3.0%) of the CP children.

Although we did not investigate why the patients had these beliefs, we can hypothesize that patients expect to be screened for diseases ‘appropriate’ for their age. It is concerning

that, of patients who incorrectly believed that they had been tested for HIV, almost all (96%) assumed that no result communication meant a negative test. This finding has several implications. Individuals may be falsely reassured that all is well, and so would not alter potentially high-risk behaviour, and may be less likely to volunteer for a subsequent test, believing it unnecessary, both these factors potentially contributing to delayed MI-503 cost HIV diagnoses. Over 80% of patients stated that they would agree in principle to routine preoperative HIV testing. Such screening may be beneficial in young,

otherwise fit patients, for whom an elective orthopaedic procedure may be the only medical contact they have over a prolonged period, and in patients who do not perceive themselves to be at risk, notably, those in older age groups [10]. Our observation that patients older than 50 years were less likely to believe Selleck GSK3 inhibitor that they had been tested for HIV and less likely to accept routine preoperative testing than younger patients goes tuclazepam against emerging trends in HIV epidemiology. In England, Wales and Northern Ireland, the number of adults aged 50 years and older with diagnosed HIV infection has more than tripled

between 2000 and 2007, and rates of late presentation are high (48%) [11]. Often patients have consulted several medical practitioners prior to their HIV diagnosis, suggesting that earlier diagnosis could, and should, have been possible [12]. To our knowledge, this is the first study examining patient understanding of preoperative blood tests in the context of HIV screening and patient acceptance of HIV testing prior to surgery. We found one study examining HIV screening in the orthopaedic setting [13], conducted before the advent of highly active antiretroviral therapy, where the emphasis was on surgeon safety rather than patient well-being. Another strength of our study is that we compared patient attitudes towards preoperative HIV screening with those for other chronic conditions. It is interesting that attitudes towards routine HIV testing and screening for diabetes or high cholesterol among our patients did not differ significantly, when many doctors and public health policy-makers still regard HIV testing as very different from testing glucose or cholesterol [14].

This mismatch suggests that neurofunctional reorganization occurs with age, allowing the brain to compensate for the various structural losses. A possible answer to this mismatch has been captured by Stern (2009) in his concept of ‘cognitive reserve’. The

notion of cognitive reserve refers to the existence of an ability to optimize performance that supports cognition in healthy, high-performing older individuals. The neural bases of these cognitive abilities would either be forced to make optimal use of an existing neural network (neural reserve) or, alternatively or concurrently, would engage neural networks normally not engaged in this given cognitive ability (neural compensation). As revealed by neuroimaging, neural reserve appears to be associated with enhanced Lapatinib in vivo activations of areas or networks known to be associated with a given cognitive ability, whereas neural compensation appears as relying on the activation of areas or networks not normally known to be associated with this cognitive ability. Thus, for Stern (2009) the notion of cognitive reserve would account for the paradox NVP-BEZ235 purchase posed by the degradation of the physical brain on one hand vs. the preservation of cognitive abilities in some older individuals on the other hand. In support of the general concept of cognitive reserve, neurofunctional

reorganization phenomena have been reported in neuroimaging studies of young and older individuals whose performance levels remain high. These phenomena have been interpreted according to several forms of neurofunctional reorganization posited to occur in healthy cognitive aging. Cabeza (2002) observed that elderly individuals who had maintained a given cognitive ability were characterized by the presence of

patterns Dynein of activation that were bilateral as opposed to more lateralized activations in younger high-performing individuals as well as older, less performing, individuals. This pattern was interpreted as suggesting that age-related hemispheric asymmetry reductions may have a compensatory function by engaging additional brain areas, such as homologous contralateral regions (Reuter-Lorenz & Lustig, 2005; Reuter-Lorenz & Cappell, 2008; Reuter-Lorenz & Park, 2010). Other studies that examined the hemispheric distribution of attentional resources (Banich, 1998) supported this explanation (Reuter-Lorenz et al., 1999; Reuter-Lorenz & Lustig, 2005; Ansado et al., 2009). Together, these studies show a shift in efficiency from within- to across-hemisphere processing with aging in order to maintain performance. These results suggest that elderly adults use both hemispheres to process information in relatively easy tasks whereas young adults do so only for tasks that are more difficult.

, 2001). This ED pathway, in which the phosphorylation step is postponed, is also probably used by the other members of the carbohydrate-utilizing group. In this pathway, glucose is oxidized via gluconate to 2-keto-3-deoxygluconate and then phosphorylated to 2-keto-3-deoxy-6-phosphogluconate, selleck compound which is further split into pyruvate and glyceraldehyde-3-phosphate (Tomlinson

et al., 1974). In addition, other steps in common metabolic pathways may have special modifications in the halophilic Archaea, such as the production of acetate by an ADP-forming acetyl-CoA synthetase (Siebers & Schönheit, 2005). Halobacterium does not grow on sugars, but its growth is stimulated by the addition of carbohydrates to the medium (Oren, 2002b), where

glucose can be transformed into gluconate (Sonawat et al., 1990). Oxidation of carbohydrates is often incomplete and is usually associated with the production of acids (Hochstein, 1978). In the presence of glycerol, some species of the genus Haloferax and Haloarcula produce Carfilzomib solubility dmso acetate, pyruvate, and d-lactate (Oren & Gurevich, 1994). Production of d-lactate, acetate, and pyruvate from glycerol by the haloarchaeal communities of the Dead Sea and saltern crystallization ponds has also been observed. In these environments, acetate is poorly utilized (Oren, 1995). Analysis of the genome of the flat square archaeon Progesterone Hqr. walsbyi showed a few unique features. One of them is the presence of a gene cluster that allows uptake of phosphonates and subsequent cleavage of the carbon–phosphorus bond by a phosphonate lyase. Another is the possible use of dihydroxyacetone as a carbon and energy source after its uptake via a phosphoenol pyruvate-dependent phosphotransferase system (Bolhuis et al., 2006). Growth studies showed that, indeed, Hqr. walsbyi could metabolize dihydroxyacetone (Elevi Bardavid & Oren, 2008). Based

on the analysis of its genome, this species can also grow on pyruvate and glycerol (Bolhuis et al., 2006). Its apparent inability to take up glycerol, as shown in an analysis of the natural community in a saltern crystallizer pond in Mallorca (Rosselló-Mora et al., 2003) remains unexplained. A food chain is thus possible, in which glycerol produced as an osmotic solute by the alga Dunaliella is converted in part to dihydroxyacetone by extremely halophilic bacteria of the genus Salinibacter (Bacteroidetes). Haloquadratum and other members of the Halobacteriaceae (Elevi Bardavid & Oren, 2008; Elevi Bardavid et al., 2008) can then take up the dihydroxyacetone and the remainder of the glycerol. Some representatives of the family can metabolize aliphatic and aromatic hydrocarbons and long-chain fatty acids, such as hexadecanoic acid (Bertrand et al., 1990; Oren, 2006; McGenity, 2010a).

Residual antibacterial activity was determined by a disk diffusion assay against P. aeruginosa. The effect of pH was determined using a pH range from 2 to 10 with diluted HCl or NaOH. After incubation for 2 h at 25 °C and neutralization to pH 7, the residual activity was tested. Resistance to proteases was tested by incubating Seliciclib S07-2 compound with proteinase K, trypsin or α-chemotrypsin at ratios of 1 : 10 and 1 : 5 (w/w) as described previously (Tabbene et al., 2009a). MS experiments were carried out using a prOTOFTM instrument (Perkin-Elmer) operating in the reflectron mode and with an accelerating voltage

of 16 kV. The matrix used was α-cyano-4-hydroxycinnamic acid. The instrument was calibrated with peptides of known molecular mass in the 1000–2500-Da range (PepMix1, LaserBiolabs, France). In typical measurements, the mass accuracy was ±5 p.p.m. The MIC of the S07-2 compound on different bacterial strains was determined by microbroth dilution assay. Twofold increasing concentrations of the selleck chemicals llc sample (from 3.9 to 1000 μg mL−1) were tested on cell suspensions (106 CFU mL−1) in LB medium. Control wells with 20% methanol were included. Plates were incubated at 37 °C

for 24 h. Bacterial growth was determined by measuring the OD600 nm using a microplate reader (Bioteck, ELx 800). MIC was defined as the lowest concentration inhibiting bacterial growth. MBC was determined from the same experiments by removing 10 μL from wells without growth after 48 h of incubation. These aliquots were then spread onto LB agar plates for counting. MBC was defined as the lowest concentration causing 95% killing of the microbial population. The hemolytic activity of the S07-2 compound on human erythrocytes was also determined (Mangoni et al., 2000). Briefly, blood was centrifuged AMP deaminase and erythrocytes were washed three times with 0.9% NaCl. Increasing concentrations of the sample, ranging from 3.9 to 1000 μg mL−1, were incubated with the erythrocyte suspension (1 × 107 cells mL−1 in 0.9% NaCl) at 37 °C for 30 min. The extent of hemolysis was measured at 415 nm. Hypotonically

lysed erythrocytes were used as a standard for 100% hemolysis. The S07-2 compound was subjected to chemical assays, to investigate its siderophore nature. Catecholate-, hydroxamate- and carboxylate-type siderophores were measured according to Arnow (1937), Neilands (1981) and Shenker et al. (1992), respectively. Fe2+-chelating activity was evaluated according to Moktan et al. (2008). Twofold increasing concentrations of the S07-2 compound (0.24–125 μg mL−1) were added to 0.5 mM ferrous chloride tetrahydrate solution. After a 5-min incubation at room temperature, 1.25 mM ferrozine was added. The mixture was incubated for 10 min at room temperature and the A562 nm was measured. EDTA was used as a positive control.