Moreover, this would additionally provide further insight into whether exogenous attention and IOR are independent or interrelated mechanisms. In summary, behavioural performance showed facilitation of expected targets in the endogenous tasks and IOR in the exogenous task. The electrophysiological results demonstrated early effects of exogenous attention followed by later endogenous

attention modulations. These effects were independent in both the endogenous predictive learn more and exogenous tasks. However, voluntarily directing attention away from a cued body part influenced the early exogenous marker (N80). This suggests the two mechanisms are interdependent, at least when task demands require more demanding

shifts of attention. The early marker of exogenous tactile attention, the N80, was not related to Palbociclib in vivo the IOR effect shown behaviourally. Although the neural markers of IOR remain elusive, at least in regard to the sense of touch, we conclude exogenous attention and IOR are not necessarily two sides of the same coin. The authors have no conflict of interests to declare. Abbreviations EEG electroencephalography ERP event-related potential HEOG horizontal electro-oculogram IOR inhibition of return ITI inter-trial interval RT response time SOA stimulus-onset asynchrony “
“The baroreceptor reflex controls spontaneous fluctuations in blood pressure. One major control variable of the baroreflex is the sympathetic vasoconstrictor activity to muscles [MSNA; burst frequency (BF) and burst incidence (BI)], which can be quantitatively assessed by microneurography. We aimed to investigate the central regions involved in baroreflex regulation of MSNA. Healthy men (mean

age 25 years) ID-8 participated in three experimental sessions. (i) Microneurography recordings of MSNA from the left peroneal nerve during rest and baroreflex unloading, induced by lower body negative pressure (LBNP; −40 mmHg). If MSNA could be reliably recorded throughout this procedure (n = 15), the subjects entered the positron emission tomography (PET) experiments. The two PET sessions took place in a randomised order. Cerebral glucose metabolism (18-fluorodeoxyglucose) was analysed after: (ii) baroreflex unloading (LBNP); and (iii) control condition (lying in the LBNP chamber without suction). The PET data were analysed employing SPM8. LBNP elicited a significant increase in MSNA in all successfully recorded subjects (BI: P = 0.001; F = 5.54; BF: P < 0.001; F = 36.59). As compared with the control condition, LBNP was associated with increased PET regional glucose metabolism bilaterally in the orbitofrontal cortex (OFC; BA 11, 47). Related to the rise of BF, there was increased activation of the left OFC (BA 11); related to the rise of BI there was increased activation of the brainstem corresponding to the rostral ventrolateral medulla.

The activity was measured by decreasing the A340 nm based on the transformation of vanillin to vanillic acid. Influence on latent absorbance by the production of NAD(P)H was adjusted by molar extinction coefficients. Calculations were based on molar extinction coefficients

of vanillin (10.6 × 103; pH 7) and NAD(P)H (6.30 × 103) at 340 nm. The reaction mixture comprised 100 mM KPB, 5 mM NAD(P)+, and 0.25 mM vanillin at the final concentration. The other method investigated the enzyme’s substrate specificity and the effect of pH or temperature on it. KU-60019 Enzyme activity was determined by quantification of corresponding oxidized products from aromatic aldehydes by HPLC as described above. The reaction mixture (1.0 mL) comprised 100 mM appropriate buffer, 5 mM NAD(P)+, 2.5 mM substrates, and 0.23 and

0.26 U of purified VDH from Micrococcus sp. TA1 and B. cepacia TM1, respectively. The reaction mixture was incubated for 20 min at an appropriate temperature, after which the reaction was stopped by adding 0.2 mL of Opaganib order 0.5 N HCl. The acid produced was quantified by HPLC. One unit of enzyme activity was defined as the amount of enzyme that catalyzes the transformation of 1 μmol of vanillin to vanillic acid. The enzyme from Micrococcus sp. TA1 that catalyzes the dehydrogenation of vanillin was purified from cells as follows: after cultivation on 2 g L−1 vanillin as a carbon source with each liquid medium as described in Materials and methods, cells were harvested by centrifugation (10 000 g, 10 min, 4 °C). The pellet was resuspended in 50 mM KPB (pH 7.5) and the suspension was treated Decitabine with an ultrasonicator (201 M sonicator; Kubota, Tokyo, Japan) at 9 KHz and 170 W for 15 min; the utmost care was taken to maintain the temperature below 5 °C. The lysate was then centrifuged at 16 000 g for 20 min. The resulting supernatant was used as the cell extract. The cell extract dialyzed against 10 mM Tris-HCl buffer (pH 8.5) was applied to a 100 mL DEAE-Sepharose FF column (GE Healthcare Bio-Science, Buckinghamshire, UK). The enzyme was eluted with a

linear gradient of increasing NaCl concentration (0–0.5 M, total volume 1.5 L). The fractions with VDH activity were pooled. NaCl (2 M) was added with gentle stirring to the pooled fraction, and this solution was applied to a 30-mL butyl-Sepharose column (GE Healthcare Bio-Science). The enzyme was eluted using a gradient of decreasing NaCl concentration (2–0 M, total volume 600 mL). The active fractions were dialyzed against 10 mM Tris-HCl buffer (pH 8.5). The dialyzed enzyme solution was applied to a 1-mL Resource Q column (GE Healthcare Bio-Science). The enzyme was eluted with a linear gradient of increasing NaCl concentration (0–0.5 M, total volume 100 mL). The enzyme from B. cepacia TM1 was purified from the cell extract as follows: the cell extract of B.

The activity was measured by decreasing the A340 nm based on the transformation of vanillin to vanillic acid. Influence on latent absorbance by the production of NAD(P)H was adjusted by molar extinction coefficients. Calculations were based on molar extinction coefficients

of vanillin (10.6 × 103; pH 7) and NAD(P)H (6.30 × 103) at 340 nm. The reaction mixture comprised 100 mM KPB, 5 mM NAD(P)+, and 0.25 mM vanillin at the final concentration. The other method investigated the enzyme’s substrate specificity and the effect of pH or temperature on it. find more Enzyme activity was determined by quantification of corresponding oxidized products from aromatic aldehydes by HPLC as described above. The reaction mixture (1.0 mL) comprised 100 mM appropriate buffer, 5 mM NAD(P)+, 2.5 mM substrates, and 0.23 and

0.26 U of purified VDH from Micrococcus sp. TA1 and B. cepacia TM1, respectively. The reaction mixture was incubated for 20 min at an appropriate temperature, after which the reaction was stopped by adding 0.2 mL of Ruxolitinib 0.5 N HCl. The acid produced was quantified by HPLC. One unit of enzyme activity was defined as the amount of enzyme that catalyzes the transformation of 1 μmol of vanillin to vanillic acid. The enzyme from Micrococcus sp. TA1 that catalyzes the dehydrogenation of vanillin was purified from cells as follows: after cultivation on 2 g L−1 vanillin as a carbon source with each liquid medium as described in Materials and methods, cells were harvested by centrifugation (10 000 g, 10 min, 4 °C). The pellet was resuspended in 50 mM KPB (pH 7.5) and the suspension was treated anti-EGFR antibody with an ultrasonicator (201 M sonicator; Kubota, Tokyo, Japan) at 9 KHz and 170 W for 15 min; the utmost care was taken to maintain the temperature below 5 °C. The lysate was then centrifuged at 16 000 g for 20 min. The resulting supernatant was used as the cell extract. The cell extract dialyzed against 10 mM Tris-HCl buffer (pH 8.5) was applied to a 100 mL DEAE-Sepharose FF column (GE Healthcare Bio-Science, Buckinghamshire, UK). The enzyme was eluted with a

linear gradient of increasing NaCl concentration (0–0.5 M, total volume 1.5 L). The fractions with VDH activity were pooled. NaCl (2 M) was added with gentle stirring to the pooled fraction, and this solution was applied to a 30-mL butyl-Sepharose column (GE Healthcare Bio-Science). The enzyme was eluted using a gradient of decreasing NaCl concentration (2–0 M, total volume 600 mL). The active fractions were dialyzed against 10 mM Tris-HCl buffer (pH 8.5). The dialyzed enzyme solution was applied to a 1-mL Resource Q column (GE Healthcare Bio-Science). The enzyme was eluted with a linear gradient of increasing NaCl concentration (0–0.5 M, total volume 100 mL). The enzyme from B. cepacia TM1 was purified from the cell extract as follows: the cell extract of B.

“
“The transcriptional repressor Rex has been implicated in the regulation of energy metabolism and fermentative growth in response to redox potential. Streptococcus mutans, the primary causative agent of human dental caries, possesses

a gene that encodes a protein with high similarity to members of the Rex family of proteins. In this study, we showed that Rex-deficiency compromised the ability of S. mutans to cope with oxidative stress and to form biofilms. The Rex-deficient mutant also accumulated less biofilm after 3 days than the wild-type strain, especially when grown in sucrose-containing Rapamycin datasheet medium, but produced more extracellular glucans than the parental strain. Rex-deficiency caused substantial alterations in gene transcription, including those involved in heterofermentative metabolism, NAD+ regeneration and oxidative stress. Among the upregulated genes was gtfC, which encodes glucosyltransferase C, an enzyme primarily responsible for synthesis of water-insoluble glucans. These results reveal that Rex plays an important role in oxidative stress responses and biofilm formation by S. mutans. Streptococcus mutans lives selleck kinase inhibitor almost exclusively in biofilms on the tooth surface, an environment that experiences dramatic fluctuations in nutrient

availability, pH and oxygen tension. As the primary etiological agent of human dental caries, triclocarban the ability to survive various harsh challenges in the oral cavity is known to be critical to its pathogenicity (Burne, 1998). While the molecular mechanisms that govern carbohydrate utilization, acid production and low pH adaptation by this microorganism are well-studied

(Abranches et al., 2008; Lemos & Burne, 2008; Zeng & Burne, 2008), limited information is available concerning oxygen metabolism and oxidative stress and their impact on the expression of virulence traits by S. mutans. Streptococcus mutans lacks a complete respiratory chain and does not normally carry out oxidative phosphorylation, but the organism has a high capacity to metabolize oxygen (Marquis, 1995). When grown on the tooth surface, S. mutans must cope with various oxidative stress conditions, including damaging reactive oxygen species (ROS) and unfavorable cellular redox potential (Marquis, 1995). ROS, such as •O2−, HO•, and H2O2, are produced inside the bacterial cells when growing in an aerobic environment. ROS are toxic as they are highly reactive and can cleave RNA/DNA and oxidize essential proteins and lipids. It was recently shown that aeration significantly decreased the ability of S. mutans to form biofilms (Ahn & Burne, 2007; Ahn et al., 2007). Notably, growth in the presence of oxygen dramatically altered the cell surface, affecting hydrophobicity and the localization of glucosyltransferases B and C (Ahn et al., 2007).

“
“The transcriptional repressor Rex has been implicated in the regulation of energy metabolism and fermentative growth in response to redox potential. Streptococcus mutans, the primary causative agent of human dental caries, possesses

a gene that encodes a protein with high similarity to members of the Rex family of proteins. In this study, we showed that Rex-deficiency compromised the ability of S. mutans to cope with oxidative stress and to form biofilms. The Rex-deficient mutant also accumulated less biofilm after 3 days than the wild-type strain, especially when grown in sucrose-containing selleck compound medium, but produced more extracellular glucans than the parental strain. Rex-deficiency caused substantial alterations in gene transcription, including those involved in heterofermentative metabolism, NAD+ regeneration and oxidative stress. Among the upregulated genes was gtfC, which encodes glucosyltransferase C, an enzyme primarily responsible for synthesis of water-insoluble glucans. These results reveal that Rex plays an important role in oxidative stress responses and biofilm formation by S. mutans. Streptococcus mutans lives Midostaurin molecular weight almost exclusively in biofilms on the tooth surface, an environment that experiences dramatic fluctuations in nutrient

availability, pH and oxygen tension. As the primary etiological agent of human dental caries, Y-27632 2HCl the ability to survive various harsh challenges in the oral cavity is known to be critical to its pathogenicity (Burne, 1998). While the molecular mechanisms that govern carbohydrate utilization, acid production and low pH adaptation by this microorganism are well-studied

(Abranches et al., 2008; Lemos & Burne, 2008; Zeng & Burne, 2008), limited information is available concerning oxygen metabolism and oxidative stress and their impact on the expression of virulence traits by S. mutans. Streptococcus mutans lacks a complete respiratory chain and does not normally carry out oxidative phosphorylation, but the organism has a high capacity to metabolize oxygen (Marquis, 1995). When grown on the tooth surface, S. mutans must cope with various oxidative stress conditions, including damaging reactive oxygen species (ROS) and unfavorable cellular redox potential (Marquis, 1995). ROS, such as •O2−, HO•, and H2O2, are produced inside the bacterial cells when growing in an aerobic environment. ROS are toxic as they are highly reactive and can cleave RNA/DNA and oxidize essential proteins and lipids. It was recently shown that aeration significantly decreased the ability of S. mutans to form biofilms (Ahn & Burne, 2007; Ahn et al., 2007). Notably, growth in the presence of oxygen dramatically altered the cell surface, affecting hydrophobicity and the localization of glucosyltransferases B and C (Ahn et al., 2007).

All data were entered into Epi-Data 3.1 (The EpiData Association, Odense, Denmark) with in-built logic and range checks and analysed in Stata 11.0 (Statacorp, College Station, TX). Characteristics of women with and without a history of lifetime IPV were compared using a χ2 test for categorical variables and the Kruskal−Wallis test for continuous variables. Any variables found to be associated with lifetime IPV in univariable analysis (P < 0.2) were

then entered into a mulitivariable logistic regression model to obtain adjusted odd ratios Selleck Venetoclax (AORs) and 95% confidence intervals (CIs). Ethical approval was obtained from the South East London Research Ethics Committee 4 (reference number 11/H0807/7). Between May and December 2011, 440 women attended the clinic. We excluded 16 women from recruitment because of intercurrent severe mental health problems and a further 110

were not approached by their clinician. Of 314 women invited to participate, 198 (63%) consented to take part. Of these, seven had data missing on IPV and our analysis was therefore based on the remaining 191 women. Nearly two-thirds of the participants (114 of 179) stated that they wanted their questionnaire answers to be shared with their clinic doctor. This was not associated with lifetime experience of IPV (P > 0.5). The median age of participants was 38 years (range 21–71 years). Within this sample, HSP inhibitor 70% of participants were African-born Black, 20% were of other Black ethnicity, 6% were White and 4% were of other ethnicity. Almost all participants (97%) had documented heterosexual risk for HIV infection and there were no injecting drug users (IDUs). A minority of participants (30 of 191) had a CD4 count of < 350 cells/μL. The prevalence of reported lifetime IPV in this study population was 51.8% (99 of 191; 95% CI 44.7–59.0%). IPV within the past 1 year was reported by 14.1% of women (27 of 191; 95% CI 9.1–19.1%). Lifetime experience of

IPV while pregnant was reported by 14.1% of participants (27 of 191; 95% CI 9.1–19.1%). The most common form of IPV experienced by women was humiliation/emotional abuse (45%) followed by feeling afraid of a partner Baf-A1 mw (33%), physical abuse (33%) and then rape/sexual abuse (20%) (Fig. 2). On univariable analysis, we found associations between lifetime IPV and younger age, other Black ethnicity, history of mental health problems, being unemployed, leaving education aged < 16 years, not having enough money to cover basic needs, a history of transactional sex, childhood physical and sexual abuse, and sexual debut aged < 16 years (all P < 0.05; Tables 1, 2 and 3). In the multivariable logistic regression model, we found an association between younger age and lifetime IPV after adjusting for all other significant variables, with each year increase in age associated with an 8% decrease in odds of having experienced IPV (AOR 0.92; 95% CI 0.86–0.97; P < 0.001; Table 4).

All data were entered into Epi-Data 3.1 (The EpiData Association, Odense, Denmark) with in-built logic and range checks and analysed in Stata 11.0 (Statacorp, College Station, TX). Characteristics of women with and without a history of lifetime IPV were compared using a χ2 test for categorical variables and the Kruskal−Wallis test for continuous variables. Any variables found to be associated with lifetime IPV in univariable analysis (P < 0.2) were

then entered into a mulitivariable logistic regression model to obtain adjusted odd ratios Selleckchem Alpelisib (AORs) and 95% confidence intervals (CIs). Ethical approval was obtained from the South East London Research Ethics Committee 4 (reference number 11/H0807/7). Between May and December 2011, 440 women attended the clinic. We excluded 16 women from recruitment because of intercurrent severe mental health problems and a further 110

were not approached by their clinician. Of 314 women invited to participate, 198 (63%) consented to take part. Of these, seven had data missing on IPV and our analysis was therefore based on the remaining 191 women. Nearly two-thirds of the participants (114 of 179) stated that they wanted their questionnaire answers to be shared with their clinic doctor. This was not associated with lifetime experience of IPV (P > 0.5). The median age of participants was 38 years (range 21–71 years). Within this sample, MG-132 concentration 70% of participants were African-born Black, 20% were of other Black ethnicity, 6% were White and 4% were of other ethnicity. Almost all participants (97%) had documented heterosexual risk for HIV infection and there were no injecting drug users (IDUs). A minority of participants (30 of 191) had a CD4 count of < 350 cells/μL. The prevalence of reported lifetime IPV in this study population was 51.8% (99 of 191; 95% CI 44.7–59.0%). IPV within the past 1 year was reported by 14.1% of women (27 of 191; 95% CI 9.1–19.1%). Lifetime experience of

IPV while pregnant was reported by 14.1% of participants (27 of 191; 95% CI 9.1–19.1%). The most common form of IPV experienced by women was humiliation/emotional abuse (45%) followed by feeling afraid of a partner 4��8C (33%), physical abuse (33%) and then rape/sexual abuse (20%) (Fig. 2). On univariable analysis, we found associations between lifetime IPV and younger age, other Black ethnicity, history of mental health problems, being unemployed, leaving education aged < 16 years, not having enough money to cover basic needs, a history of transactional sex, childhood physical and sexual abuse, and sexual debut aged < 16 years (all P < 0.05; Tables 1, 2 and 3). In the multivariable logistic regression model, we found an association between younger age and lifetime IPV after adjusting for all other significant variables, with each year increase in age associated with an 8% decrease in odds of having experienced IPV (AOR 0.92; 95% CI 0.86–0.97; P < 0.001; Table 4).

Thus, multimer formation seems to be an additional means, besides

copy number reduction and ssDNA accumulation, by which loss of genetic elements ensuring click here efficient lagging strand synthesis may cause plasmid destabilization. This work was supported by the Lower Austrian State Academy. M.K. received a fellowship from the Higher Education Commission of Pakistan. “
“The Streptococcus bovis/Streptococcus equinus complex (SBSEC) comprises pathogenic species associated with different degrees with human infections but also spontaneously fermented dairy products. We aimed therefore at developing a specific identification assay for the SBSEC targeting the 16S rRNA gene comprising a multiplex PCR followed by a differentiating Venetoclax concentration restriction fragment length polymorphisms (RFLP). The multiplex PCR assay was positively applied on 200 SBSEC isolates including reference strains. The assay did not yield false-positive amplifications with strains of closely related bacteria and isolates of non-SBSEC streptococci, lactococci, enterococci, and other genera of dairy origin. The downstream RFLP using

MseI and XbaI enabled further discrimination of Streptococcus infantarius/S. bovis (biotype II.1) from Streptococcus gallolyticus (biotype I and II.2)/Streptococcus alactolyticus and S. equinus. Furthermore, the newly developed primers can be used directly for Sanger sequencing. Conclusively, this novel PCR/RFLP assay is applicable in the complex dairy microbial communities and provides an important tool to assess the prevalence of members of the SBSEC in dairy products. The Streptococcus bovis/Streptococcus equinus complex (SBSEC) comprises a large variety of species and subspecies of which especially Streptococcus infantarius subsp. infantarius and potentially other members of the SBSEC were reported as the predominant lactic acid bacteria (LAB) in spontaneously

fermented African milk products (Abdelgadir et al., 2008; Wullschleger, 2009; Jans, 2011). Members of the SBSEC were also detected in Mexican, Greek, and Italian cheese, fermented Mexican maize drink, or fermented Bangladeshi milk (Tsakalidou et al., 1998; Díaz-Ruiz et al., 2003; Pacini et al., 2006; Rashid et al., 2009; Renye et al., 2011). First discrimination of SBSEC has been Lonafarnib solubility dmso based on phenotypic classification schemes that were greatly revised with the ability of 16S rRNA gene phylogenetic analysis (Poyart et al., 2002; Schlegel et al., 2003). The genes sodA (Poyart et al., 1998, 2002) and groESL (Chen et al., 2008) were targeted for PCR assay in combination with sequencing and restriction fragment length polymorphism (RFLP) for the identification of members of the SBSEC. A further assay was developed specifically for Streptococcus gallolyticus subsp. macedonicus based on the 16S rRNA gene (Papadelli et al.

pIJ702-rshAbldG was constructed by inserting a bldG cassette prepared by PCR (primers

are shown in Supporting Information, Table BGJ398 manufacturer S1) between the PstI and KpnI sites of pIJ702-rshA. The bldG cassette contained its own promoter region, which directed the expression of the coding sequence. For genetic complementation, the 957-bp DNA fragment containing the bldG coding sequence (cds) and its promoter region was amplified by PCR using the primers GCF/GCR and cloned between the EcoRI and HindIII sites of pKU463 to form pBG. pBG was then introduced into the bldG mutant by transformation to generate a kanamycin-resistant transformant carrying the plasmid integrated at the K38-1 site (nucleotide sequence accession no. AB251919). Disruption of bldG was carried out by a homologous recombination technique based on REDIRECT technology (Gust et al., 2003). The cosmid clone SGR1G10 used for bldG knockout in S. griseus containing the region corresponding to nucleotides 3874894–3914177 in the SCH727965 genome sequence database was obtained in our study using SuperCos1 (Stratagene, Japan,

Tokyo) as a vector. An apramycin resistance gene cassette was prepared by PCR using the primers DisGF/DisGR and used for the replacement for the bldG cds by in vivo recombination using λ RED. The resulting apramycin-resistant cosmids purified from Escherichia coli GM2163 were introduced into the wild-type strain of S. griseus. Apramycin-resistant recombinants were then screened and checked for true recombination by PCR using appropriate primer sets. All mutants obtained exhibited the identical bald phenotype; hence, one of them was designated as the bldG mutant. The transcriptional activities of the promoters preceding the rshA-sigH operon (PH1, the σH-dependent promoter), sigN (PN1), and rpp operon (Prpp) were studied by S1 protection analysis. Methods and conditions for RNA preparation and S1 nuclease mapping were previously

described (Kieser et al., 2000; Kelemen et al., 2001; Takano et al., 2007). The probes for PH1, PN1, and Prpp were prepared by PCR using primers HS1-F/HS1-R* for PH1, NS1-F/NS1-R* for PN1, and RS1-F/RS1-R* for Prpp, respectively (primers indicated with an asterisk were labelled at its 5′-end selleck chemical with [γ-32P] ATP using T4-polynucleotide kinase). Preparation of a C-terminally histidine-tagged RshA (RshA-6xHis) was described previously (Takano et al., 2003). For preparation of RshA carrying an N-terminal glutathione-S-transferase (GST-RshA), an rshA cassette was amplified using the PCR primers Rex-F/Rex-R and cloned between the BamHI/EcoRI sites of pGEX-4T-2 (GE Healthcare, Tokyo, Japan). For BldG-6xHis, a bldG cassette was amplified using primers Gex-F/Gex-R and cloned between the NdeI/HindIII sites of pET26-b+ (Takara Shuzo). The E.

An agar drop buy Quizartinib containing a putative attractant or repellent was placed around the centre of a flow chamber and the behaviour of free-swimming cells was analysed under a microscope. MAA showed that L. biflexa cells gradually accumulated around an agar drop that contained an attractant such as glucose. Leptospira cells often spin without migration by transformation of their cell body. The frequency at which cells showed no net displacement decreased with a higher glucose concentration, suggesting that sensing an attractive chemical allows these cells to swim more smoothly. Investigation of the chemotactic behaviour of

these cells in response to different types of sugars showed that fructose and mannitol induced negative chemotactic responses, whereas xylose and lactose were non-chemotactic for L. biflexa. The MAA developed in this study can be used to investigate other chemoattractants and repellents. “
“The cellulase-producing fungal strain Y-94, isolated in Japan and invalidly described as Acremonium cellulolyticus nom. nud. strain Y-94, seldom forms Napabucasin concentration enteroarthric conidia under nutrient starvation conditions. Phylogenetic analysis using ITS1-5.8S-ITS2 and RNA polymerase II large subunit gene sequences revealed that strain Y-94 is closely related to Talaromyces, given that these Y-94 sequences showed 100% identity with those of Talaromyces pinophilus NBRC 100533T. By

contrast, the identity between β-tubulin-encoding Non-specific serine/threonine protein kinase genes from strain Y-94 and T. pinophilus NBRC 100533T was 98.1%. Morphological

and phenotypic differences between these strains in colony color, conidiophore formation, and cellulase productivity were observed. Together, these data indicated that strain Y-94 belonged to the genus Talaromyces. We propose that strain Y-94 is a new species, Talaromyces cellulolyticus, on the basis of morphology and molecular evidence. The ex-holotype is Y-94 (= FERM BP-5826, CBS 136886 [holotype] TNS-F-48752). “
“It is widely accepted that antibiotics provide a critical selective pressure for the horizontal transfer of antibiotic resistance between bacterial species. This study demonstrated that a combination of low doses of kanamycin and streptomycin, which inhibited the growth of recipient and donor cells, respectively, had positive effects on the transmission of the conjugation plasmids pRK2013, pSU2007, and RP4 from Escherichia coli DH5α to HB101 at their minimum inhibitory concentrations (MICs). Administration of either antibiotic alone as well as other antibiotics in combination or alone did not have this effect. Two-dimensional electrophoresis revealed that 60 proteins were downregulated and 14 proteins were upregulated in the conjugation of E. coli DH5α (pRK2013) and HB101 in the presence of kanamycin and streptomycin. Of these proteins, 64 were subsequently identified by mass spectrometry.