Although few data are available for patients receiving cancer chemotherapy

or prolonged high-dose corticosteroids (>20 mg od prednisolone for more than 2 months) where the prognosis is >1 year, it may be reasonable to give isoniazid prophylaxis to all those with a positive www.selleckchem.com/screening/pi3k-signaling-inhibitor-library.html IGRA who do not have active TB. Individuals with a positive interferon-γ assay but no clinical or radiological evidence of active TB are assumed to have latent infection. Active TB should be excluded with a detailed history and examination and at least a chest radiograph. Other investigations might be necessary, for example lymph node biopsy (if lymphadenopathy), or colonoscopy and biopsy (if diarrhoea). It is especially important to consider subclinical TB prior to starting HAART because of the risk of IRIS [207] (see also ‘IRIS’). Alternatives for treating latent TB: isoniazid for 6 months [201]; [A11] Shorter courses using other drugs have been tried to help overcome poor adherence. Rifampicin plus pyrazinamide given daily or twice weekly for 2 months has been used successfully in HIV-positive patients [200,203,204] but is not recommended [DII] because in largely non-HIV-infected patients it has been associated with severe or fatal hepatic reactions in at least 50 cases in the United States [208]. Studies in areas of high TB prevalence have shown selleck screening library that

isoniazid prophylaxis Dolichyl-phosphate-mannose-protein mannosyltransferase post-treatment achieves short-term reductions in rates of TB [209,210]. Such a strategy may in fact prevent reinfection,

which is more common than true reactivation in such settings [211]. For maximum benefit the isoniazid would need to be continued long-term, or at least until CD4 cell count had substantially risen on HAART, and there are no data to support such an approach. It is clear that relapse rates are lower in patients on HAART, associated with both improved CD4 cell counts and achieving an undetectable viral load [212]. Post-treatment TB prophylaxis is therefore not recommended, but HAART should be continued. [DII] Guidelines for prevention and control of transmission of TB include: NICE: Tuberculosis, clinical diagnosis and management of TB, and measures for its prevention and control, 2006. These are available at: http://www.dh.gov.uk/en/Publichealth/Communicablediseases/Tuberculosis/index.htm In summary, for good control of TB there should be: recognition that TB is a potential diagnosis; Hospital care of patients with potential or known TB requires: appropriate isolation of patients; TB is a notifiable disease in the United Kingdom, as it is in many other countries. If the patient is concerned about disclosure of HIV status following notification by an HIV physician, then the notification can be done by any physician involved in clinical care.

2b). Comparisons with known lipopolysaccharide profiles from other gram-negative bacteria suggests that the LMW band corresponds to the rough lipopolysaccharide (lipid A plus core) and the HMW bands to the smooth lipopolysaccharide (complete lipopolysaccharide molecules with different number of attached O-antigen units) (Choudhury et al., 2005; Vilches et al., 2007). The mutant did not produce the smooth lipopolysaccharide bands and showed faint LMW lipopolysaccharide bands with

different electrophoretic mobility from the parental bands (Fig. 2b). The results indicated that BM07-59 was damaged in the production of normal lipopolysaccharide. These buy LY294002 results were not unexpected, as the galU mutants in Pseudomonas aeruginosa and Aeromonas hydrophila produced truncated lipopolysaccharide core and lacked the O-antigen (Choudhury et al., 2005; Vilches et al., 2007). UDP-glucose formed through the GalU catalyzed reaction can serve as glucose donor for core and O-antigen polysaccharide biosynthesis in the production of lipopolysaccharide (Dean & Goldberg, 2002). To determine why the O-antigen is missing in BM07-59, we analyzed the composition of lipopolysaccharide from wild-type and mutant strains grown in M1 medium containing 70 mM fructose at 30 °C. Purified lipopolysaccharide from wild type and BM07-59 is predominantly

composed of a lipid, with 10.7% and 3.5% of the lipopolysaccharide MG-132 purchase composed of carbohydrate, respectively. The carbohydrate fraction of lipopolysaccharide from wild-type strain contained rhamnose, xylose, mannose, glucose, N-acetyl glucosamine and 3-deoxy-d-manno-oct-2-ulsonic acid (KDO) in a mole ratio of 31.8 : 1.7 : 0.3 : 50.2 : 14.9 : 1.1, respectively, whereas the carbohydrate fraction of lipopolysaccharide

from BM07-59 contained rhamnose, glucose, N-acetyl glucosamine and KDO in a mole ratio of 3.9 : 11.2 : 30.8 : 54.1, respectively. Thus, in comparison with the wild-type lipopolysaccharide, the lipopolysaccharide from BM07-59 contained a much smaller molar amount of rhamnose and glucose but a much larger (50-fold) molar amount of KDO was detected in the mutant lipopolysaccharide. Dynein This significant sugar compositional difference of lipopolysaccharide between wild-type and mutant strains clearly reflects the fact that BM07-59 is unable to supply UDP-glucose for O-antigen and core lipopolysaccharide synthesis. To further confirm that galU gene is involved in lipopolysaccharide and exobiopolymer production, a complementary assay was performed. Plasmid pBBR-KT galU harboring galU gene from P. putida KT2440 was introduced into BM07-59 to recover GalU activity. As expected, the complement BM07-59 (KT GalU) restored the parental phenotype for colony morphology (Fig. 1a), autoagglutination phenotype (Fig. 2a), exobiopolymer production (Fig. 1b) and lipopolysaccharide synthesis (Fig. 2b). These results indicated that the expression of galU gene from P.

Methods  Details of all unprevented and prevented dispensing incidents occurring over 3 months (September–December

2005) at five district general hospitals across Wales were reported and analysed using a validated method. Rates of unprevented and prevented dispensing Raf inhibitor incidents were compared using Mann–Whitney U test. Reported error types, contributory factors and clinical significance of unprevented and prevented incidents were compared using Fisher’s exact test. Key findings  Thirty-five unprevented and 291 prevented dispensing incidents were reported amongst 221 670 items. The rate of unprevented (16/100 000 items) and prevented dispensing incidents (131/100 000 items; P = 0.04) was significantly different. There was a significant difference in the proportions of prevented and unprevented dispensing incidents involving the wrong directions/warnings on the label (prevented, n = 100, 29%; unprevented, n = 4, 10%; P = 0.02) and the wrong drug details on the label (prevented, n = 15, check details 4%; unprevented, n = 6, 14%; P = 0.01). There was a

significant difference in the proportions of prevented and unprevented dispensing incidents involving supply of the wrong strength (prevented, n = 46, 14%; unprevented, n = 2, 5%; P = 0.02) and issue of expired medicines (prevented, n = 3, 1%; unprevented, n = 5, 12%; P = 0.002). Conclusion  The use of prevented dispensing incidents as a surrogate marker for unprevented incidents is questionable. There were significant differences between unprevented and prevented dispensing incidents in terms of rate and error types. This is consistent with the medication error iceberg. Care must be exercised when extrapolating prevented dispensing incident data on error types to unprevented dispensing incidents. “
“Objective  To explore stakeholder perspectives on a government-subsidised Home Medicines Review (HMR) service and factors affecting the uptake of HMRs for older residents of retirement villages in Australia.

Urease Methods  Thirty-two in-depth interviews and four focus groups were undertaken with a purposive sample of 32 residents of retirement villages, 10 pharmacists, nine general practitioners (GPs) and a general practice nurse. Data were transcribed verbatim and analysed using the framework approach. Key findings  Three major themes were identified: participants’ perceptions of the HMR service, barriers to the uptake of HMRs and strategies for increasing the uptake of HMR. Residents had positive, negative or mixed perceptions, whereas health professionals were generally positive about the benefits of the service. Barriers to the uptake of HMRs were related to GPs, pharmacists, patients and the healthcare system. A strategy recommended by multiple stakeholders for increasing the uptake of HMRs was to use a multi-faceted intervention targeting residents and their health professionals.

In addition, two meetings Forskolin cost with patients and community representatives

were held to discuss and receive feedback and comment on the proposed guideline recommendations. The first was held before the Writing Group’s consensus meeting and the second as part of the public consultation process. The GRADE Working Group [3] has developed an approach to grading evidence that moves away from initial reliance on study design to consider the overall quality of evidence across outcomes. BHIVA has adopted the modified GRADE system for its guideline development. The advantages of the modified GRADE system are (i) the grading system provides an informative, transparent summary for clinicians, patients and policy makers by combining an explicit evaluation of the strength of the recommendation with a judgement of the quality of the evidence for each recommendation, and GSK2118436 concentration (ii) the two-level grading system of recommendations has the merit of simplicity and provides clear direction to patients, clinicians and policy makers. A Grade 1 recommendation is a strong recommendation to do (or not do) something, where the benefits clearly

outweigh the risks (or vice versa) for most, if not all patients. Most clinicians and patients should and would want to follow a strong recommendation unless there is a clear rationale for an alternative approach. A strong recommendation usually starts with the standard wording ‘we recommend’. A Grade 2 recommendation is a weaker or conditional recommendation,

where the risks and benefits are more closely balanced or are more uncertain. Most clinicians and patients would want to follow a weak or conditional recommendation but many would not. Alternative approaches or strategies may be reasonable depending on the individual patient’s circumstances, preferences and values. A weak or conditional recommendation usually starts with the standard wording ‘we suggest’. The strength of a recommendation is determined not only by the quality of evidence for defined outcomes but also the balance between Thalidomide desirable and undesirable effects of a treatment or intervention, differences in values and preferences and, where appropriate, resource use. Each recommendation concerns a defined target population and is actionable. The quality of evidence is graded from A to D and for the purpose of these guidelines is defined as the following. Grade A evidence means high-quality evidence that comes from consistent results from well-performed randomized controlled trials (RCTs), or overwhelming evidence of some other sort (such as well-executed observational studies with consistent strong effects and exclusion of all potential sources of bias). Grade A implies confidence that the true effect lies close to the estimate of the effect.

12,13 Because no stool samples could be collected for the control period, it cannot be determined with certainty that the diarrhea symptoms are caused by the viral pathogens detected in the samples at the symptomatic time point. Indeed, asymptomatic carriage of enteric viruses such as norovirus is frequent during outbreaks.14 Moreover, virus shedding in feces could be prolonged after infection. For norovirus, detection for

up to 2 weeks after the end of symptoms is not rare.15 However, clinical symptoms were consistent with viral infection. One third of patients presented vomiting, which is more frequent in viral gastroenteritis, particularly noroviruses, than in enteroinvasive diarrhea due to bacteria.16,17 Our results confirm the high incidence rate of diarrhea in French forces in N’Djamena as observed see more by the epidemiological surveillance. However, the incidence rate was lower than usually observed (588 cases per 1,000 person-years vs 1,428 per 1,000 person-years in 2007). This difference may be due to the study period. Indeed, French forces surveillance data derived from the past 10 years in Chad have shown that there is a drastic increase in diarrhea during the humid season, whereas our study corresponded to the dry season. The seasonal impact on the incidence

rate of TD has already been described in others’ studies.18,19 Seasonal variation is consistent with enteric virus outbreaks, as is usually observed PD0325901 solubility dmso in industrialized countries.20 Further studies are needed to determine if there is also a seasonal activity of enteric viruses in Chad. The fact that eating outside the mess (ie, in local restaurants

or in field kitchens) constituted a risk factor for diarrhea may be due to unsafe food handling and serving practices, usually considered at risk for TD.21 Soldiers spending time off-base had the same potential contact with endemic pathogens as any other traveler.22 The protective effect of eating in a temporary encampment is likely related to the predominant use of prepackaged meals in these facilities. The protective effect of prepackaged food is also corroborated by the decreased incidence of diarrhea observed when soldiers were restricted to their quarters and consumed only prepackaged meals in February 2008.3,23 The multivariate analysis underlined the protective aminophylline effect of always eating at the military mess. This supports the positive effects of the Hazard Analysis and Critical Control Point programs in such structures, which improve food handling and hygiene. In addition, we found subjects to have a fourfold risk of diarrhea if a case of diarrhea was already present in their close circle. As a group effect has been eliminated, this corresponds to a high risk of person-to-person transmission. This is a new insight into TD, and is probably related to the high frequency of enteric viruses identified.

4A). The supernatant was further centrifuged at 10,000 g for 10 min and the pellet was separated on a sucrose density gradient (0.32, 0.8 and 1.2 m sucrose), and the synaptosome learn more fraction was obtained between 0.8 and 1.2 m sucrose. For the postsynaptic density (PSD) fraction, the synaptosome sample was further solubilized with 0.5% Triton X-100 and the pellet, after centrifugation at 200 000 g for 1 h, was suspended with 40 mm Tris–HCl pH 8.0 and 1% sodium dodecyl sulfate (SDS). Protein samples from homogenate (20 μg), synaptosome (3 μg) and PSD (2 μg) fractions were loaded onto each lane and subjected to SDS-polyacrylamide gel electrophoresis (SDS-PAGE) for Western blotting

(Fig. 4A). Signal intensities of immunoreacted bands were determined by densitometric measurement using ImageJ software (available from the US National Institutes of Health) and normalized with actin signal intensities. Statistical significance was assessed by two tailed, one-sample t-test using PRISM (GraphPad Software, San Diego,

CA, USA). All results are expressed as mean ± SEM. Under deep pentobarbital anesthesia (100 mg/kg of body weight, i.p.), mice were perfused transcardially with 4% paraformaldehyde Afatinib concentration in 0.1 m sodium phosphate buffer (PB; pH 7.2) for light microscopic immunohistochemistry or with 4% paraformaldehyde and 0.1% glutaraldehyde in 0.1 m PB for postembedding immunogold electron microscopy. Brains to be compared simultaneously were embedded in single paraffin blocks, and paraffin sections (4 μm in thickness) were made using a sliding microtome (SM1000R; Leica, Nussloch, very Germany). Microslicer sections were also used for immunofluorescence (50 μm; VT1000S, Leica) and for postembedding

immunogold (400 μm). All immunohistochemical incubations were done at room temperature. For light microscopic immunohistochemistry, paraffin sections were first subjected to pepsin pretreatment for antigen exposure, i.e., incubation in 1 mg/ml of pepsin (DAKO, Carpinteria, CA, USA) in 0.2 N HCl for 10 min at 37°C. Then sections were incubated successively with 10% normal donkey serum for 20 min, primary antibodies (1 μg/ml) overnight, biotinylated secondary antibodies for 2 h and avidin–biotin–peroxidase complex for 1 h, using a Histofine SAB-PO(R) kit (Nichirei Corp., Tokyo, Japan). Immunoreaction was visualized using the tyramide signal amplification kit (Perkin-Elmer, Boston, MA, USA). To detect nonsynaptic AMPA receptors, double immunofluorescence without pepsin pretreatment was done for GLAST and GluA1 or GluA4 using microslicer sections. Images of whole brain sections were taken with a dissecting microscope, while those of cerebellar cortex were with a confocal laser scanning microscope (FV1000; Olympus). For postembedding immunogold, cerebellar slices were cryoprotected with 30% sucrose in 0.1 m PB, and frozen rapidly with liquid propane in a Leica EM CPC unit.

The fixation point was a red (R255 G0 B0) square (0.67 × 0.67°); the directional cue was a red (R255 G0 B0) arrow (0.67 × 0.67°); targets were white (R255 G255 B255) figure 8s (0.62 × 1°); discrimination symbols were white (R255 G255 B255) Es or 3s (0.62 × 1°);

distractors were white (R255 G255 B255) 2s or 5s (0.62 × 1°). Targets were located at the four corners of an imaginary square, each 5.4° diagonally from the central fixation point. Each block of trials started with a check of the calibration quality and, if required, a two-dimensional 13-point re-calibration procedure covering the display area. At the beginning and end of each recording, a sequence of reflexive saccades was recorded to provide data for post hoc assessment and adjustment of the calibration if required. Stimuli were presented using PsychoPy, an open-source experimental control NU7441 software package (Peirce, 2007, 2008). All participants attended two testing sessions. At the first session, after a 6-m visual acuity test with the Snellen wall chart (each subject was required to have visual find more acuity of no worse than 6/12 corrected in their best eye), each participant’s vision was checked whilst they were seated in front of the computer screen with the chin supported

by the chinrest of the recording column. At a viewing distance of 600 mm, some participants’ own corrective lenses were not suitable. A range of corrective lenses of various strengths was then tried until the best possible acuity at 600 mm was achieved. Vision was then tested again with an array of symbols at

the size and contrast actually used in the experiments. The actual test and recording started after calibration of the eye movement recording system. At the first session, subjects first performed two blocks of the saccade task ‘without discrimination’, and then two blocks of the saccade task ‘with Progesterone discrimination’. The saccade task ‘without discrimination’ was always performed at the start of the first session, while participants were not yet aware of the potential relevance of the symbol-changes. Another two blocks of the task ‘with discrimination’ were performed at the second session, 1 week after the first session. In the task ‘with discrimination’, each trial was followed by a visual prompt asking the participant whether E or 3 had appeared. Participants responded E or 3 with a right or left manual button press, respectively. Participants were explicitly told to guess if unsure of the answer. They were also told that on some trials there would be no discrimination symbol, and to push one of the two buttons at random when they thought no discrimination symbol had appeared. In No-change and Distractor trials there was no discrimination symbol, but subjects were not told about the different symbol-change conditions or the likelihood of a discrimination symbol occurring.

As we discuss later, the IL12B region is also associated with TAK. These data strongly suggest that ustekinumab would be a very promising therapeutic option for patients with TAK. The only established genetic component associated with TAK has been HLA-B52. The association between HLA-B*52:01 and TAK has been repeatedly shown in different populations.[33-38] There are studies reporting the importance of other alleles, including HLA-DPB1

or HLA-DRB1 alleles.[39, 40] The recent genome-wide association study (GWAS) showed an independent association in the HLA-DQB1/DRB1 locus.[41] Although HLA-B51, a strong susceptibility allele to Selleckchem PF-2341066 Behçet disease,[42] shares large parts of amino acid sequencing with HLA-B*52:01, the association between HLA-B51 and TAK was negatively reported.[34] Our recent work might provide an answer to these observed different susceptibilities.[38] Our study indicates the importance of the 67th and 171st amino acid residues for TAK susceptibility where the 67th is one of the CFTR modulator two amino acid residues not shared between HLA-B*51:01 and *52:01. Furthermore, both the amino acid positions are located at peptide binding grooves,[43-45] suggesting that peptide binding at these positions would be very important for the predisposition of the two different autoimmune diseases. A previous Mexican study suggested

the involvement of the 63rd and 67th amino acids.[46] Thus, different studies suggest the importance of the 67th amino acid of the HLA-B protein. Although HLA-B39 was reported to be associated with severe complications of TAK as well as TAK onset in a previous study,[47] the association was not observed in a recent Japanese study, and it did not find a different association between

HLA-B67:01 and TAK clinical manifestations.[48] Our recent work confirmed this lack of association Progesterone of HLA-B39 and the positive association of HLA-B*67:01.[38] HLA-B*67:01 has not been reported in Turkey and Middle-East Asia. Although GCA shows association with HLA-DR4,[49] which is not a TAK susceptibility allele, meta-analysis of TAK and GCA would reveal similarity and differences between the two large vessel arterites. Recently, we reported the first GWAS results for this disease at the same time as a US/Turkish group.[41, 50] Both groups reported IL12B as a strong susceptibility locus to TAK. Our group also reported the MLX region in chromosome 17 and a US/Turkish group reported the FCGR2A/3A region as another susceptibility locus. The US/Turkish group also reported the PSMG1 region as a suggestive locus. Our data also showed that the polymorphism in the IL12B region is associated with high incidence of AR, severity of AR and higher time-averaged CRP level as a representative of disease activity. Furthermore, our data indicated that the polymorphism of the IL12B region displayed a synergistic effect on TAK susceptibility in combination with HLA-B*52:01.

These photos have been previously reported to activate monkey amygdalar neurons (Tazumi et al., 2010). The facial photos, obtained using five human models, consisted of three head orientations: straight ahead (frontal face); 30° to the right (profile face); and 30° to the left (profile face). The frontal faces consisted of three gaze directions (directed toward, and averted to the TGF-beta inhibitor left or right of the monkey), and the profile faces comprised two gaze directions (directed toward, and averted to the right and left of the monkey).

The facial stimuli were 256 digitized color-scale images. Stimuli were presented on a black background of 0.7 cd/m2 with their centers at the center of the display. The luminance of each stimulus was determined by measuring luminance of the circular area (radius, 6.35 cm) including each stimulus inside the circle by means of a luminance meter (BM-7A; Topcon, Tokyo). The luminance of these stimuli ranged from 1.36 to 3.66 cd/m2 [luminous intensity (total luminance) ranged from

16.4 to 44.2 mcd]. We did not use facial stimuli ABT 737 with profiles rotated by 30° to the right and gaze direction averted to the right, or profiles rotated by 30° to the left and gaze direction averted to the left. In these facial stimuli, it is difficult to detect the dark iris; only the white sclera could be seen. In monkey faces, the iris can always be recognized as it occupies the major part of the visible eye. Therefore, this type of human facial stimuli appears to be unusual for monkeys. In addition, the iris can be recognized in all of the frontal faces, much regardless of gaze direction, whereas in these particular profiles the iris cannot be recognized. The lack of the iris produces a qualitative difference among the facial stimuli. For these reasons,

we avoided profiles without a visible iris. Figure 1B shows line drawings of faces with three gaze directions (cartoon faces), eye-like patterns and face-like patterns (J1–4) that newborn babies orient toward (Johnson et al., 1991). The luminance of the white and black areas inside these illustrations was 36.5 and 0.7 cd/m2, respectively (total luminance of the cartoon faces, eye-like patterns and face-like patterns were 38.7, 188.6 and 179.3 mcd, respectively). In addition, as control stimuli, four simple geometric patterns (circle, cross, square and star) were used. Luminance of the white areas inside the simple geometric patterns was 36.5 cd/m2 (total luminance of the circle, cross, square and star were 151.6, 96.0, 188.1 and 61.0 mcd, respectively). The cartoon faces, eye-like patterns and face-like patterns comprised 256 digitized RGB images; the four simple geometric patterns comprised 256 digitized images. These stimuli were displayed on a CRT monitor with a resolution of 640 × 480 pixels, and the size of the stimulus area was 5–7 × 5–7°. Some of the pulvinar neurons were further tested with scrambled images of the stimuli that elicited the strongest responses.

Recently, the importance of Calothrix rhizosoleniae has been acknowledged as open ocean symbionts in a variety of diatoms (Foster et al., 2010). Nevertheless, to date no estimate of the overall influence in the C and N cycles of the genera within Rivulariaceae has been attempted and questions remain open regarding their phylogenetic organization. Strains examined in this study were isolated from natural populations such as microbial mats, microbialites and rocky shore biofilms, summarized in Table 1. Unicyanobacterial cultures were obtained from enrichment cultures, and individual tapering filaments with heterocysts were picked using light microscopy

(Axioscope 40, Carl Zeiss, Germany). Individual cultures were grown in

50- or 100-mL flasks in an incubation chamber at an average temperature of 29 °C, 14/10 light/dark cycles (Pozas Azules), 18 °C, 12/12 light/dark cycles Selleck CAL101 (Askö) and 28 °C, 12/12 light/dark cycles (Heron Island). All cultures were grown in 50–100 μE m−1 s−1. Cultures were transferred to new media lacking reduced forms Navitoclax of nitrogen every 3 weeks. DNA was extracted from individual cultures (approximately 500 μL) that were incubated overnight at 50 °C with 10 × extraction buffer (20 mM Tris-HCl, pH 7.5–8.2, 50 mM EDTA, 20 mM NaCl) and proteinase K (final concentration 0.25 mg mL−1). Proteins and lipids were separated with two phenol and one chloroform extraction and DNA was precipitated with sodium acetate (3 M) and absolute ethanol, followed by a 45-min incubation at −20 °C. DNA pellets were stained with GlycoBlue™ (Ambion, Austin, TX) and resuspended in water. A fragment consisting of almost the complete 16S rRNA gene, the intergenic transcribed spacers and part of the 23S rRNA gene was amplified from all strains using universal primer 27F (5′AGA GTT AGA GTT TGA TCM TGG CTC AG 3′) (Lane, 1991) and cyanobacteria-specific B23S (5′CTT CGC CTC TGT GTG CCT AGG T 3′) (Gkelis et al., 2005). The amplification reaction had a final volume of 50 μL with

1 × reaction buffer, 2.5 mM MgCl2, 0.2 mM dNTPs, 0.6 μM of each primer and 5 U Taq DNA polymerase. The thermal cycle included an initial denaturalization at 94 °C for 2 min, followed by 25 cycles of 94 °C Racecadotril for 45 s; 54 °C for 45 s; 68 °C for 2 min and a final extension of 30 min at 68 °C. The PCR products obtained (approximately 1800 bp) were gel-extracted (Qiagen, Austin, TX) and sequenced. Sequences were obtained on a capillary sequencer (Applied Biosystems Avant-100) with five reactions including primers 27F, 1492R (5′TAC GGY TAC CTT GTT ACG ACT T 3′) (Lane, 1991) and B23S (Gkelis et al., 2005). Sequences were assembled and aligned with sequencher 3.1.1 (Gene Codes Corporation, Ann Arbor, MI), and identified with the Greengenes dataset (http://greengenes.lbl.gov/cgi-bin/nph-index.cgi) with basic local alignment search tool (blast).