A total of 1098 files for HIV-positive patients who attended the HIV out-patient clinic of the Department of Clinical Immunology and Rheumatology at the Medical University Hanover for at least one visit between January 2004 and December 2010 were screened for the presence of a diagnosis of SpA. A cross-sectional study was conducted to investigate aberrancies in Forskolin cost T-cell

homeostasis induced by HIV-1 in these subjects. The prevalence of SpA in the HIV-positive patients was 1.6% (18 of 1098). Interestingly, the percentage of patients with SpA who were human leucocyte antigen (HLA)-B27 negative in our HIV-positive cohort was 80%. Despite combination antiretroviral therapy (cART) and viral suppression, an incomplete immune recovery of T-cell naïve/memory distribution and turnover, as identified by intracellular Ki-67 expression,

was observed in HIV-positive patients with SpA. Independent of HLA-B27 status and despite cART, HIV-positive patients can develop SpA and exhibit an increased T-cell turnover rate. “
“3.1 We recommend patients are given the opportunity to be involved in making decisions about their treatment. GPP 4.1 We recommend patients with chronic infection start ART if the CD4 cell count is ≤350 cells/μL: it is important not to delay treatment initiation if the CD4 cell count is close to this threshold. 1A   We recommend patients with the following conditions start ART:   ● AIDS diagnosis [e.g. Kaposi sarcoma (KS)] irrespective of CD4 cell count. 1A ● HIV-related selleck chemical co-morbidity, including HIV-associated nephropathy (HIVAN), idiopathic thrombocytopenic purpura, symptomatic HIV-associated neurocognitive (NC) disorders irrespective of CD4 cell count. 1C ● Coinfection

with hepatitis B virus (HBV) if the CD4 cell count is ≤500 cells/μL (see Section 8.2.2 Hepatitis B). 1B ● Coinfection with hepatitis C virus (HCV) if the CD4 cell count is ≤500 cells/μL (Section 8.2.3 Hepatitis C). 1C ● Non-AIDS-defining malignancies requiring immunosuppressive radiotherapy or chemotherapy (Section 8.3.2 When to start ART: non-AIDS-defining malignancies). Reverse Transcriptase inhibitor 1C We suggest patients with the following conditions start ART:   ● Coinfection with HBV if the CD4 cell count is >500 cells/μL and treatment of hepatitis B is indicated (see Section 8.2.2 Hepatitis B). 2B 4.2 We recommend patients presenting with an AIDS-defining infection, or with a serious bacterial infection and a CD4 cell count <200 cells/μL, start ART within 2 weeks of initiation of specific antimicrobial chemotherapy. 1B 4.3 We recommend patients presenting with primary HIV infection (PHI) and meeting any one of the following criteria start ART:   ● Neurological involvement. 1D ● Any AIDS-defining illness. 1A ● Confirmed CD4 cell count <350 cells/μL. 1C 4.

Majority of caries-active children had maxillary incisor caries, and the presence of dental caries in the maxillary incisors carried a high odds ratio for the child to have caries in the rest of the dentition. This caries pattern is not unique to this study EX 527 purchase and has been demonstrated in other studies[20, 21]. Alaluusua et al.[16] reported that visible plaque on the labial surfaces of maxillary incisors could predict the caries status of very young children (sensitivity: 83%; specificity: 92%). The results of

this study confirmed that an assessment of the presence of caries and the plaque accumulation of the 4 maxillary incisors may serve as an alternative to a full oral examination especially during public health epidemiology studies and be utilized by physicians and mid-level healthcare providers to detect caries in young children. At the time of the study, very few Singaporean children had been to a dentist. Furthermore, these children visited the dentist

only because they had dental decay requiring attention. Thus, this practice was not protective in the caries risk assessment, but rather appeared to be a consequence of the child having dental decay. In contrast selleck kinase inhibitor to only 1% in Singapore, 37% of Hong Kong parents indicated that the first dental visit for their child should be around 1 year of age[22]. The American Academy of Pediatric Dentistry recommends that all children should have their first dental visit no later than 12 months of age[23]. old Many Singaporean parents were unaware of the appropriate age for their child to have their first dental visit and felt that a visit to the dentist was warranted only if their child had tooth pain. Of those who reported an age, 5 years was thought by many parents to be an appropriate time for their child’s first dental visit in our study. Many parents cited

that their child did not require regular dental check-ups because they did not complain about their teeth. Homecare practices also appeared to be poor; close to 40% of children were brushing their teeth without supervision, a practice that is not aligned with the AAPD guidelines[24]. These worrisome attitudes and practices suggest that the establishment of a dental home at an early age was not a priority for Singaporean parents. Currently, the school dental health programme in Singapore provides free dental examination and treatment for school children (7 years of age and older), and this may have influenced parental perception on the appropriate age to visit the dentist. Additionally, there were no formalized public health dental services for toddlers and preschool children, which may explain the low awareness of the merits of preventive dental visits and subsequent utilization rate among preschool children.

Seroepidemiologic studies of influenza among well-returned travelers indicate seroconversion in 2.8%,6 and among febrile returning travelers, the incidence of influenza is estimated to be between 5 and 15%.13 Thus, our findings likely represent a significant underestimate of cases of influenza among ill-returned travelers. High hospitalization rates potentially indicate that only more severe infections find more were evaluated at a GeoSentinel site, thereby further underestimating the burden of influenza in travelers. Third, during influenza season in temperate countries, confirmatory diagnostic tests are not often sent once influenza is circulating within a community,

and this study included only confirmed or probable diagnoses. Fourth, absence of immunization history limits our ability to quantify true potential influenza preventability in this cohort. Fifth, given the short incubation period of influenza, we cannot exclude the possibility that some travelers, especially those returning home during their influenza R428 supplier season, or residing in the tropics or ESEACN, became infected en

route home or after travel. Influenza acquired abroad versus from the country of residence would be impossible to distinguish clinically. Finally, our data do not permit estimation of incidence rates or destination-specific numerical risks for influenza.7,14 This is the single largest analysis of latitudinal patterns of influenza in travelers, to date, and is derived from a multicenter, heterogeneous population, reflecting the spectrum of travel demographics and destinations over a 10-year period. Alternate hemisphere and out-of-season influenza vaccine availability may benefit a small proportion of travelers. As noted previously, while knowledge of influenza prevention among travelers appears to be good, translation of this knowledge into uptake of prevention measures such as vaccination, antiviral prophylaxis, and hand hygiene among travelers remains low.15,16 Proportionate morbidity estimates by region of travel

can inform pre-travel consultation and emphasize the Y-27632 2HCl ease of acquisition of infections such as influenza during travel. These data can inform broad-level decision-making in travel medicine, public health, and health care policy. GeoSentinel: the Global Surveillance Network of the International Society of Travel Medicine is supported by Cooperative Agreement U50/CCU412347 from the Centers for Disease Control and Prevention. The funding source (the Centers for Disease Control and Prevention) had no role in study design, data analysis and interpretation, or in writing the manuscript. A. K. B., F. v. S., P. L. L., E. S., and M. E. W. state that they have no conflicts of interest to declare. F. C. has received an honorarium to attend the Tamiflu Advisory Board once in 2006. P. G. was sponsored by Sanofi-Pasteur to attend conferences. J. T.

We analyzed travelers in the GeoSentinel Surveillance Network7,8 to determine latitudinal travel patterns in those who acquired influenza abroad. We also sought to elucidate the frequency of cross-hemispheric influenza acquisition in travelers during years of NH and SH vaccine mismatch. The GeoSentinel Surveillance Network comprises 54 travel/tropical medicine clinics on six continents, which contribute anonymous, clinician- and questionnaire-based travel data on ill travelers to a centralized database;7,8 for additional details see www.geosentinel.org. The questionnaire learn more constitutes prospectively established variables of interest, including

demographic and travel-related data, reason for most recent travel, inpatient or outpatient status, pre-travel history, and limited clinical information. Final diagnoses are Inhibitor Library screening assigned by a physician from a standardized list

of >500 etiologic or syndromic diagnoses.7,8 Returning travelers who attended a GeoSentinel clinic between April 1997 and December 2007, and whose final diagnosis was probable or confirmed were eligible for analysis.2 Persons traveling for immigration or who sought care during travel were excluded. Influenza” represented infections with either influenza A or influenza B virus. To assign a “confirmed” diagnosis in GeoSentinel, best available national reference diagnostics are used according to applicable regional and national standards. In the case of influenza, this would include biological confirmation by one or more of direct fluorescent antigen detection, cell culture with immunofluorescent antigen detection, or nucleic-acid amplification testing such as polymerase chain reaction (PCR). A probable diagnosis of influenza would be restricted to patients with classical presentation (ie, fever plus one or more respiratory

symptoms such as Pyruvate dehydrogenase cough, dyspnea, coryza, or sore throat) and exposure history with laboratory exclusion of competing etiologies.7 Returning travelers assigned a final diagnosis of “influenza-like illness” were excluded to capture only those cases of influenza with a higher degree of diagnostic certainty, as noted above. Countries in northern or southern temperate regions were defined as having latitude ≥23° N or ≥23° S, respectively, and an epidemiologic pattern of seasonal influenza circulation. “Tropical” countries were defined as those at latitude <23° N or <23° S with potential year-round circulation of influenza. Countries spanning temperate and tropical regions (eg, China), were classified based on most likely region of exposure according to most populous cities and highly frequented airports. Cross-hemispheric travelers were those who embarked from one hemisphere with seasonal influenza circulation to another, regardless of layovers.

2, inset lane 5). These results suggest that the anti-Candida compounds belong to the iturin group characterized GSK126 manufacturer by the presence of tyrosine residue and a lipid-soluble β-amino fatty acid (Peypoux et al., 1981; Besson & Michel, 1986; Stein, 2005; Volpon et al., 2007). The molecular masses of the three lipopeptide compounds were determined by MALDI-TOF/MS. The spectrum mass of a1, a2 and a3 showed homologues (M+Na)+ major peaks at m/z 1053.5, 1067.5 and 1081.5, respectively, suggesting that these compounds are homologue molecules exhibiting different

lengths in their fatty acid chain (CH2=14 Da). Moreover, the molecular masses of these anti-Candida compounds are very close to C14, C15 and C16 homologues of bacillomycin D described in previous reports (Peypoux et al., 1984; Moyne et al., 2001; Koumoutsi et al., 2004; Oleinikova et al., 2005). These results confirmed the presence of the bamC gene involved in the synthesis of bacillomycin D in B. subtilis B38 strain. The MIC and MFC values of the purified compounds were evaluated

against host pathogenic Candida strains and were compared with those of amphotericin B (Table 3). The most potent compound a3 containing 16 carbons in its fatty acid moiety had MFC values superior to those of amphotericin B against most pathogenic C. albicans species. Furthermore, a3 showed a twofold lower MFC value (59.07 μM) than that of amphotericin B (135.26 μM) against the pathogenic-resistant C. albicans sp. 311 FN. The compound a2 containing 15 carbons in the fatty acid moiety exhibited a moderate anti-Candida HKI-272 clinical trial activity and was two- to Fluorouracil mw eightfold less active than a3. Moreover, compound a1, having the shortest fatty acid chain (14 carbons), showed a weak anti-Candida effect and was 8–32-fold less active than a3. Differential sensitivity of C. albicans toward these compounds could be related to the length of the acyl chain. Our data

suggest a direct correlation between the length of the acyl chain of these compounds and their anti-Candida activities. Previous reports have underlined the importance of the length of the lipid moiety of bacillomycin D and bacillopeptin lipopeptides in the inhibitory effect against various fungal species (Kajimura et al., 1995; Moyne et al., 2001). Members of the iturin family generally exhibit strong antifungal activity against a wide variety of fungi, by interacting with the cytoplasmic membrane causing pore formation (Besson & Michel, 1984; Maget-Dana & Peypoux, 1994). It is tempting to speculate that differences in the activity of the anti-Candida compounds are related to the deepness of the generated membrane pores. In fact, antifungal compounds with a long acyl chain could be entirely incorporated into the yeast membrane compared to those having shorter acyl chains that presumably cannot span a membrane (Maget-Dana & Ptak, 1995).

2, inset lane 5). These results suggest that the anti-Candida compounds belong to the iturin group characterized PLX4032 molecular weight by the presence of tyrosine residue and a lipid-soluble β-amino fatty acid (Peypoux et al., 1981; Besson & Michel, 1986; Stein, 2005; Volpon et al., 2007). The molecular masses of the three lipopeptide compounds were determined by MALDI-TOF/MS. The spectrum mass of a1, a2 and a3 showed homologues (M+Na)+ major peaks at m/z 1053.5, 1067.5 and 1081.5, respectively, suggesting that these compounds are homologue molecules exhibiting different

lengths in their fatty acid chain (CH2=14 Da). Moreover, the molecular masses of these anti-Candida compounds are very close to C14, C15 and C16 homologues of bacillomycin D described in previous reports (Peypoux et al., 1984; Moyne et al., 2001; Koumoutsi et al., 2004; Oleinikova et al., 2005). These results confirmed the presence of the bamC gene involved in the synthesis of bacillomycin D in B. subtilis B38 strain. The MIC and MFC values of the purified compounds were evaluated

against host pathogenic Candida strains and were compared with those of amphotericin B (Table 3). The most potent compound a3 containing 16 carbons in its fatty acid moiety had MFC values superior to those of amphotericin B against most pathogenic C. albicans species. Furthermore, a3 showed a twofold lower MFC value (59.07 μM) than that of amphotericin B (135.26 μM) against the pathogenic-resistant C. albicans sp. 311 FN. The compound a2 containing 15 carbons in the fatty acid moiety exhibited a moderate anti-Candida click here activity and was two- to Parvulin eightfold less active than a3. Moreover, compound a1, having the shortest fatty acid chain (14 carbons), showed a weak anti-Candida effect and was 8–32-fold less active than a3. Differential sensitivity of C. albicans toward these compounds could be related to the length of the acyl chain. Our data

suggest a direct correlation between the length of the acyl chain of these compounds and their anti-Candida activities. Previous reports have underlined the importance of the length of the lipid moiety of bacillomycin D and bacillopeptin lipopeptides in the inhibitory effect against various fungal species (Kajimura et al., 1995; Moyne et al., 2001). Members of the iturin family generally exhibit strong antifungal activity against a wide variety of fungi, by interacting with the cytoplasmic membrane causing pore formation (Besson & Michel, 1984; Maget-Dana & Peypoux, 1994). It is tempting to speculate that differences in the activity of the anti-Candida compounds are related to the deepness of the generated membrane pores. In fact, antifungal compounds with a long acyl chain could be entirely incorporated into the yeast membrane compared to those having shorter acyl chains that presumably cannot span a membrane (Maget-Dana & Ptak, 1995).

15), LGN excitatory to L4 inhibitory (P = 0.0619), and TRN inhibitory to LGN excitatory (P = 0.3). The number of neurons in each area is shown in Table 2. The model contained a total of 46 926 neurons and approximately 43 million synapses. Simple and extended versions of the Izhikevich model were used to govern the dynamics of the spiking neurons in this simulation. Obeticholic Acid mw The computational efficiency of these point neurons (single compartment) makes them ideal for large-scale simulations. Izhikevich neurons are also highly realistic and are able to reproduce at least 20 different firing modes seen in the brain, which

include: spiking, bursting, rebound spikes and bursts, subthreshold oscillations, resonance, spike frequency adaptation, spike threshold variability, and bistability of resting and spiking states (Izhikevich, 2004). Inhibitory and excitatory neurons in the cortex were modeled using the simple Izhikevich model, which are described by the following equations Nivolumab in vivo (Izhikevich, 2003): (2) where v is the membrane potential, u is the recovery variable, I is the input current, and a, b, c and d are parameters chosen based on the neuron type. For regular spiking, excitatory neurons, we set a = 0.01, b = 0.2, c = −65.0 and d = 8.0 (see Fig. 4). For fast-spiking, inhibitory neurons, we set a = 0.1, b = 0.2, c = −65.0 and d = 2.0 (Fig. 4). GABAergic and cholinergic neurons in the BF were modeled as simple

Izhikevich inhibitory and excitatory neurons, respectively. LGN and TRN neurons were modeled using the extended version of the Izhikevich neuron model to account for the bursting and tonic modes of activity, which these neurons have been shown to exhibit (Izhikevich & Edelman, 2008). The equations governing these neurons are given as: (5) The equations for this extended model are similar to the previous model, except they include additional parameters, such as: membrane capacitance (C), resting potential (vr) and instantaneous

threshold potential (vt). For LGN neurons, parameters were set to: a = 0.1, c = −60, d = 10, C = 200, vr = −60 and vt = −50. For TRN neurons, parameters were set to: a = 0.015, c = −55, d = 50, C = 40, vr = −65 and vt = −45 (Izhikevich & Edelman, 2008). To simulate Bcl-w the switch between bursting and tonic mode, the b parameter, which is related to the excitability of the cell, was changed depending upon membrane potential, v. Specifically, if v < −65, b was set to 70 and the neuron would be in bursting mode (Fig. 4; bottom, right). If v > −65, b was set to 0 and the neuron would be in tonic mode (Fig. 4; bottom, left). The synaptic input, I, driving each neuron was dictated by simulated AMPA, NMDA, GABAA and GABAB conductances (Izhikevich & Edelman, 2008; Richert et al., 2011). The conductance equations used are well established and have been described in Dayan & Abbott (2001) and Izhikevich et al. (2004). The total synaptic input seen by each neuron was given by: (7) where v is the membrane potential and g is the conductance.

Wallemia sebi was grown Apoptosis Compound Library in 500-mL Erlenmayer flasks in liquid culture on a rotary shaker at 28 °C and 180 r.p.m. for 14 days (until stationary growth phase). The medium (150 mL per flask) was composed of 0.8 g L−1 complete supplement mixture (CSM; Q-Biogene Bio-Systems, France), 1.7 g L−1 yeast nitrogen base (YNB; Q-Biogene Bio Systems), 20.0 g L−1 glucose (Chemica, Croatia), 5.0 g L−1 (NH4)2SO4, and 200.0 g L−1 NaCl (Merck, Germany). The final concentration of NaCl in the growth medium was either 5% or 20%. After 15 days of incubation, the fermentation broth medium (1200 mL) was filtered (pore size, 0.8 μm). The separated mycelia were washed with 5% or 20% NaCl in distilled H2O, to remove all traces

of growth medium. These fungal mycelia were immediately freeze-dried and stored at −20 °C until the ethanol extraction. Ten milliliters of 96% ethanol was added to 1 g lyophilized dry mycelia. The mixture was extracted overnight by orbital shaking at 25 °C and then centrifuged at 10 g for 40 min, followed by centrifugation at 21 500 g for 15 min. The obtained supernatant was used in all of the biological assays. The total solids (TS) in ethanolic extract were subsequently determined

by gravimetry. The characterization of this ethanolic extract from W. sebi was performed using gas p53 inhibitor chromatography–mass spectrometry (GC/MS). This analysis by GC/MS was carried out using an Agilent 6890N/5973 GC/MSD system. The interface, source, and quadrupole temperatures were set to 280, 150, and 230 °C, respectively. An inert DB-5ms Agilent J&W column (30 m × 0.25 mm × 0.25 μm) was used, and 1 μL of the fraction to be analyzed was injected. Splitless injection was used, at a temperature of 280 °C. The oven temperature was set to 50 °C for 10 min, followed by step heating at 40 °C min−1, up to 200 °C. Acquisition was in the EI mode, with the mass range set for m/z 45–450. The identification of the compounds in the ethanolic extract was performed by comparison of peaks with the mass spectra of both the Wiley library and the NIST02 internal reference. The hemolytic activity of the ethanolic

extract from W. sebi was determined by combining 20 μL of the extract in various final concentrations many with 80 μL of suspension of bovine erythrocytes in the erythrocyte buffer [140 mM NaCl, 20 mM tris(hydroxymethyl)aminomethane (TRIS) (Merck), pH 7.4], as described by Sepčić et al. (2003). The time necessary for 50% hemolysis (t50) was determined at the end of each experiment. All experiments were performed at 25 °C and with three repeats. Twenty microliters of ethanol-dissolved oleic (C18:1), linoleic (C18:2), and palmitic acids (C16:0) in various final concentrations, both in pure solutions or combined in 1 : 1 : 1 molar ratio, was also assayed using the same procedure. All the used fatty acids were from Fluka (Germany).

The latter scenario is made more complex when enzyme induction has not yet been fully achieved, and if doubt exists, alternatives to switch to should be considered. Steady-state (14 days following the switch) ETV pharmacokinetic parameters are lowered by previous EFV intake in the case of both once-daily (Cmin was lowered by 33%) and twice-daily SCH772984 clinical trial (Cmin was lowered by 37%) administration. However, ETV concentrations have been shown to increase over time following the switch and in patients with undetectable VLs switching from EFV to ETV, standard doses of ETV can be commenced [18]. To date, no data are available on what strategy to adopt in patients with active viral replication.

Concentrations of RPV are lowered by previous EFV administration. However, 28 days after the switch, they returned to levels comparable with those when RPV was administered without previous EFV treatment, except for a 25% BMS-907351 cell line lower Cmin. Therefore, in patients with undetectable VLs switching from EFV to RPV,

standard doses of RPV can be commenced [19]. To date, no data are available on what strategy to adopt in patients with active viral replication. Because of the strong inhibitory effect of ritonavir on CYP450 3A4, it is unlikely to require a modification of the PI/r dose when switching from EFV to PI/r. Formal pharmacokinetic data are unavailable. TDM data were presented on ATV/r and showed that after stopping EFV, ATV concentrations

were above the suggested minimum effective concentration in all studied subjects [20]. Although formal pharmacokinetic data are not available, switching EFV to RAL should not lead to clinically significant consequences, as co-administration of EFV with RAL led to a moderate-to-weak reduction in RAL Cmin (21%) [21], which may persist for 2–4 weeks, after the switch very but the degree of this reduction is unlikely to be clinically meaningful. A formal pharmacokinetic study in HIV-positive individuals showed that the induction effect of EFV necessitated an increase in MVC dose to 600 mg twice daily for 1 week following the switch [22]. MVC 300 mg twice daily (standard dose) seems to be safe after this period. Although there is an absence of data, when switching from EFV to MVC plus a PI/r, it is likely that a dose of 150 mg twice daily is safe from the first day after the switch. Whether it is advisable to use MVC 150 mg once daily in this context or for how long a twice-daily dose should be used after the switch remains unknown. In patients on fully virally suppressive regimens, switching individual components of the ART combination regimen is frequently considered for several reasons, including: management of ARV drug toxicity or intolerance, desire for once-daily dosing and reduced pill burden, management of potential DDIs, patient preference and cost [1].

So far, Paenibacillus species have been reported to produce multiple antimicrobial compounds with a broad inhibition spectrum to various bacteria and fungi. The main antimicrobial compounds produced by these species are peptide antibiotics, including polymyxins, jolipeptin, gavaserin, saltavalin, fusaricidin A–D and gatavalin (Li et

al., 2007). In this work, strain B69, a new bacterial isolate from soil, was found to display significant activity against fungi, and gram-positive and gram-negative Stem Cells inhibitor bacteria. Based on the 16S rRNA gene sequence analysis as well as physiological and biochemical characterization, strain B69 was identified as Paenibacillus elgii. This study focuses on the isolation, purification and structural elucidation of the antibiotics produced by this bacterium. Moreover, some biochemical properties of these antibiotics have also been investigated. Strain B69 was isolated from the soil samples collected from the Tianmu Mountain Afatinib National Nature Reserve (Hangzhou, China). The tested bacteria and Candida albicans ATCC 10231 were kept in our lab, and the other five fungal strains were purchased from the China General Microbiological Culture Collection Center, which all belong to soil-borne pathogens (Table 1). The bacterial strains were routinely grown at 30 °C on

a nutrient agar or in a nutrient broth, with shaking (200 r.p.m.). The fungal strains were cultivated on a potato dextrose agar (PDA) at 26 °C. All the strains were stored in 20%

(v/v) glycerol at −80 °C for long-term storage. Strain B69 was observed by light microscopy to examine the morphological characteristics of cells and spores. Motility was determined using a sulfide-indole-motility medium. All the biochemical characteristics of strain B69 and the reference strain P. elgii SD17 were determined using the methods of Logan & Berkeley (1984). Growth at different temperatures (4, 10, 15, 20, 30, 40, 45, 50 °C) Y-27632 2HCl and at different pH values (5.0, 5.6, 6.0, 7.0, 8.0, 8.5, 9.0) was tested using a nutrient broth. Tolerance to NaCl was measured in a nutrient broth supplemented with 1–10% (w/v) NaCl. All assays were performed in triplicate. For the determination of the 16S rRNA gene sequence, genomic DNA was extracted using the Bacterial Genomic DNA Miniprep Kit (Axygen). The 16S rRNA gene was amplified using two universal primers as described by Wu et al. (2007). PCR amplification and DNA sequencing were conducted using the method of Wen et al. (2009). The 16S rRNA gene sequence obtained was compared with the corresponding reference sequences retrieved from GenBank databases by blast search. The 16S rRNA gene sequence of strain B69 has been deposited in GenBank under the accession number GU321104. Strain B69 was grown in the fermentation medium (1% peptone, 0.3% sucrose, 0.3% soluble starch, 0.5% NaCl, pH 7.0–7.2) at 30 °C for 24 h.