1.4 Where pegylated interferon or adefovir is being used to treat HBV in a woman who does not yet require HIV treatment who discovers she is pregnant, treatment should be switched

to a tenofovir-based HAART regimen. Grading: 1C 6.1.5 As there is no evidence of any adverse effect on maternal or neonatal health if women become pregnant while taking ART active against HBV these should be continued. Grading: 1C 6.1.6 In all HAV non-immune HBV coinfected women HAV vaccine is recommended, after the http://www.selleckchem.com/products/Bleomycin-sulfate.html first trimester, as per the normal schedule (0 and 6–12 months) unless the CD4 cell count is <300 cells/μL when an additional dose may be indicated. Grading: 1D 6.1.7 Tenofovir and emtricitabine should form the backbone of an ART regimen in naïve patients with wild-type HIV/HBV infection and no contraindication to either drug. Grading: 1B 6.1.8 If tenofovir is not currently part of HAART, it should be added. Grading: 1B 6.1.9 Lamivudine/emtricitabine HDAC inhibitor review may be omitted from the ARV regimen and tenofovir given as the sole anti-HBV agent if there is clinical or genotypic evidence of lamivudine/emtricitabine resistant HBV. Grading: 1C 6.1.10 Lamivudine or emtricitabine should not be used as the only active drug against HBV in HAART because of the likelihood of emergent HBV resistance to these agents. Grading: 1B 6.1.11 Emtricitabine has potential antiviral benefits over lamivudine, is co-formulated

with tenofovir and appears to be equally safe during pregnancy and hence is the preferred option

to be given with tenofovir in coinfection. Grading: 2D 6.1.12 Where the CD4 cell count is <500 cells/μL HAART should be continued postpartum if HBV coinfection exists because of the increased risk of HBV progressive disease. Grading: 1B 6.1.13 Where the CD4 cell count is >500 cells/μL and there is no other indication to treat HBV, consideration should be given to continuing anti-HBV treatment postpartum with HAART incorporating tenofovir and emtricitabine. Grading: 2C 6.1.14 If a decision is taken to discontinue therapy postpartum, careful monitoring of liver function DNA ligase is imperative. Grading: 2D 6.1.15 Where the CD4 cell count is >500 cells/μL and there is HBV viraemia and evidence of liver inflammation or fibrosis, HAART containing tenofovir and emtricitabine should be continued. Grading: 2C 6.1.16 Hepatitis flares that occur after HAART cessation should be treated by resumption of active anti-HBV treatment before significant liver dysfunction occurs. Grading: 2D 6.1.17 In the absence of obstetric complications, normal vaginal delivery can be recommended, if the mother has fully suppressed HIV VL on HAART. Grading: 2C 6.1.18 Neonatal immunization with or without hepatitis B immunoglobulin (HBIG) should commence within 24 h of delivery. Grading: 1A 6.2.1 On diagnosis of new HCV infection, confirmation of HCV viraemia with quantitative VL and genotype, assessment of hepatic inflammation and function and concomitant liver disease should be performed. Grading: 1C 6.2.

Blips are frequent and represent random variation around a mean undetectable VL [5-7]. Many patients have at least one at some time [8] when they are not predictive of virological failure or associated with emergent resistance in most studies [5, 9, 10]. VL assay variation and laboratory processing artefacts account for many blips (i.e. no ‘true’ increase in viral replication), which partly explains why blips do not appear to compromise long-term outcomes [9, 11-13]. However, those with sustained low-level increases

in VL run a higher risk of virological failure. Most blips http://www.selleckchem.com/products/Romidepsin-FK228.html are low level [median magnitude 79 copies/mL in one study (range 51–201)] and short lived [median 2.5 days (range 2–11.5)] [7]. In a retrospective study,

28.6% of patients, experienced VL increases from 50 to 500 copies/mL over 8 years; 71% of these were blips [8]. Review and reiteration of the importance of full adherence, as well as looking for any tolerability/toxicity issues, DDIs/food interactions, and archived resistance should take place. However, blips do not appear to be related to intercurrent illness, vaccination, baseline CD4 cell count/VL, duration of preceding suppression or level of adherence [7, 14, 15]. Therefore, it is the recommendation of the Writing Group that a VL result of 50–400 copies/mL preceded and followed by an undetectable selleck screening library VL should not be a cause of clinical concern. In the context of repeated

blips, it may then be useful to test for resistance [16, 17]. Low-level viraemia (LLV) is defined as a repeatedly detectable but low level of viraemia over a sustained period of time. For the purposes of these guidelines, <400 copies/mL is used although it is recognized that some patients have VLs up to 1000 copies/mL without development of resistance and with therapeutic drug levels. LLV is observed in up to 8% of individuals [18] and is associated with an increased risk of virological rebound (>400 copies/mL) [6, 19]. The likelihood of resuppression after LLV is greater for lower magnitudes of viraemia: 41% after two consecutive VLs >50 copies/mL compared with 12% after two VLs >200 copies/mL GBA3 [20]. LLV is associated with resistance (37% in one study [21]) that may be associated with LLV magnitude; in one analysis, maximum VL was higher in those with who developed resistance (368 vs. 143 copies/mL; P=0.008). LLV is also associated with immune activation [10]. Low-level antigenic exposure differentially affects T-cell activation and HIV-specific T-cell response. In cohort studies [19] and clinical trials [21], patients on PI/r-based ART are more likely to experience detectable viraemia than those on NNRTI. In the absence of clear data, the Writing Group believes LLV on a low-genetic barrier regimen warrants prompt regimen change.

, 2010). In the same study, it was observed that the HSP30p-mediated expression of FLO11 ORF in either BM45 or VIN13 did not generate a flocculent phenotype under either standard laboratory media or synthetic MS300 must fermentation conditions. In the present study, we demonstrate that HSP30p-FLO11-based transgenic BM45 and VIN13 wine yeast strains are capable of a novel

MI-flocculation phenotype that seems to exclusively occur under authentic red wine fermentation conditions. This flocculation phenotype selleckchem can be characterized as being partially Ca2+ dependent and Ca2+ independent. In particular, we show that HSP30p-FLO11 transgenic wine yeast strains displaying this trait were able to produce significantly clearer wines with compacted buy Z-VAD-FMK lees fractions. All yeast strains used in this study are listed in Table 1. Yeast strains were routinely cultivated at 30 °C in rich YEPD medium, containing 1% yeast

extract, 2% peptone and 2% glucose. For selection of sulphometuron methyl (SM)-resistant BM45 and VIN13 transformants, SC medium containing 0.67% YNB and 2% glucose was supplemented with 280 and 300 μg mL−1 SM (DuPont Agricultural Products, France), respectively. Yeast strains were cryopreserved in YEPD supplemented with 15% glycerol (Ausubel et al., 1995). The cell density of suitably diluted yeast cell suspensions in 100 mM EDTA was manually determined using a haemocytometer. Grapes of Vitis vinifera Merlot (200 kg) were rinsed with sulphited water, destemmed and crushed.

As a precaution, damaged grape clusters (broken or with visual microbial alterations) were discarded in order to eliminate undesirable contamination. Red grape must [24.2% sugar (glucose and fructose), 5.8 g L−1 titratable acidity and pH 5.8] was sulphited to 40 mg L−1. Evodiamine Thereafter, red grape must was batch fermented in 20-L plastic buckets containing 3 kg of Merlot grape juice that was adjusted to exactly 10 kg by the addition of a mixture consisting of grape pulp and skins. This was followed by the addition of 4 g of diammonium phosphate. Yeast precultures in YEPD were prepared and processed as described previously (Govender et al., 2008). Thereafter, wild-type and transgenic yeast inoculum populations were preacclimatized for wine fermentations by incubation at 30 °C for 4 h with shaking at 160 r.p.m. in filter (0.22 μm cellulose acetate)-sterilized 50% v/v Merlot juice diluted with distilled water. The fermentative potential of BM45 and VIN13 wild-type strains and their transgenic derivatives were assessed in triplicate. Assuming a ratio of 0.

, 2002; Kotan et al., 2009). Lactic acid bacteria (LAB) are a broad group of gram-positive, catalase-negative, non-sporulating, usually non-motile rods and cocci that utilize carbohydrates fermentatively and form lactic acid as the major end product (Onilude et al., 2005). LAB are widely used in food and feed fermentation, contributing to the hygienic safety, storage stability and attractive sensory properties (Laitila Bafilomycin A1 price et al., 2002; Savadogo et al., 2006). These bacteria are important in the biopreservation of food and feed, related mainly to the production of antimicrobial

compounds, such as organic acids, i.e. lactic and acetic acid, hydrogen peroxide, and other antimicrobial compounds as bacteriocins (Messens & De Vuyst, 2002; Prachyakij et al., 2007). There is an increasing interest to find LAB strains that are able to

limit fungal growth and consequently mycotoxin production, in this particular case of aflatoxigenic fungi (Yang & Clausen, 2005; Aryantha & Lunggani, 2007; Elsanhoty, 2008). In previous in vitro and in vivo experiments with Lactobacillus rhamnosus L60 and Lactobacillus fermentum L23 we showed that these selleck screening library strains have probiotic characteristics (Pascual et al., 2008a ,b; Ruiz et al., 2009). Both strains have widespread antimicrobial activity mainly against bacteria and yeast, although there are no studies regarding the antagonistic effect of LAB on filamentous fungi. Therefore, the aim of this study was to evaluate antifungal activity and anti-aflatoxicogenic properties of L. rhamnosus strain L60 and L. fermentum strain L23 against toxigenic species of Aspergillus section Flavi. Lactobacillus rhamnosus L60 and L. fermentum L23 strains were obtained from a culture collection of the Bacteriology Laboratory at the National University of Río Cuarto, Córdoba, Argentina. These human strains were selected from among 100 strains of Lactobacillus on the basis of their probiotic characteristics

and bacteriocinogenic ability. The purity of the strains was confirmed by Gram staining. Strains were identified by standard biochemical tests (Holt, 1994), carbohydrate fermentation profile (Nigatu et al., 2000) and using the API 50 CHL system (BioMérieux, Marcy l’Etoile, France). The identification of L. rhamnosus L60 and L. fermentum Ribose-5-phosphate isomerase L23 was confirmed by 16S rRNA gene sequence analysis, and the sequences of these strains were registered in the GenBank database system (http://www.ncbi.nlm.nih.gov/sites/entrez) under accession numbers EF495247 (1402 bp) and GQ455406 (1523 bp), respectively. Both strains were grown in De Man Rogosa Sharpe (MRS) agar (Rogosa & Sharpe, 1963) at 37 °C, under a 5% CO2 atmosphere for 24 h. They were stored at –80 °C in MRS broth containing 30% (v/v) glycerol. A total of 137 Aspergillus section Flavi strains were recovered from brewer’s grains destined for pig feed in Argentina.

However, Trichostatin A cell line considering that the rate of evolution is faster within the Erm clade than in the corresponding clusters of bacterial KsgA (Figs 1 and 2) and that the short sequences (234 amino acid positions) do not provide sufficient signal for deep-level phylogeny reconstruction, the tree

cannot be rooted unequivocally and such an apparent paralogy is considered to be an artifact caused by long-branch attraction or the lack of a phylogenetic signal. To examine the congruence of detailed branching orders of Erm and KsgA subtrees, trees were constructed separately with all the Erm methylases detected in the databases and the corresponding KsgA proteins that exist in the same or closely related species that harbor erm genes (Figs 3 and 4). Figure

3 shows that the clustering of KsgA proteins is in good accordance with selleck chemicals the typical taxonomy. In the case of Erm, the bifurcation of the main clade into two branches of the Actinobacteria and Firmicutes is consistent with that of the KsgA proteins. However, phylogenetic anomalies generated by horizontal gene transfer and duplication are recognized within the Erm clades (Fig. 4). In Fig. 4, the obvious horizontal transfers of the erm genes between phylogenetically distant bacteria are expressed as shaded boxes, and the occurrences of gene duplication are shown as shaded without boxes. It is noticeable that most of the incidents of horizontal gene transfer occurred within the clade of the Firmicutes, whereas all of the gene duplications were detected in the clade of the Actinobacteria. The comparison of the G+C content of the erm gene with that of host chromosomal DNA also supports the frequent occurrence of erm horizontal gene transfer in pathogenic bacteria, and many of these genes are related by self-transferable plasmids or transposons (Table 1). We performed a comprehensive phylogenetic analysis with extensive Erm and KsgA/Dim1 sequences found in three domains of life. The phylogenetic tree provides some insights into the origins of the erm genes with KsgA/Dim1 sequences as an appropriate outgroup. The early branching

of the Actinobacteria and Firmicutes asserts that the origin of the current erm genes in pathogenic bacteria cannot be explained by recent horizontal gene transfer from antibiotic producers. As for the origin of the present-day erm genes, those found in pathogenic bacteria may have originated from antibiotic-resistance Carnitine dehydrogenase determinants of drug-producing bacteria (Arthur et al., 1987). If this belief is true, the main Erm clade of the Actinobacteria should be the precursor of the monophyletic tree of the Erm methylases. However, the phylogenetic tree did not place the origin of the erm genes at the ancestral node of the Actinobacteria, implying that an antibiotic producer might not provide antibiotic-resistance genes in pathogens. However, considering the frequent occurrences of horizontal erm gene transfer (Brisson-Noel et al., 1988; Berryman and Rood, 1995; Gupta et al.

diphtheriae KCTC3075 has been characterized (Kim et al., 2010), which is the orthologue of DIP0543 C. diphtheriae NCTC Veliparib 13129 (Fig. 4), confirming that this organism has both normal sialidase but also a reported trans-sialidase activity (Mattos-Guaraldi et al., 1998). Other data suggested that C. diphtheriae harbours sialic acid on its cell envelope (Mattos-Guaraldi

et al., 1999). This could originate from the trans-sialidase activity moving sialic acid directly from host sialoglycans onto the bacterium’s surface. Both the lack of association of the sialidase with production of the diphtheria toxin (Warren & Spearing, 1963; Moriyama & Barksdale, 1967) and the lack of a need for uptake for cell surface modification were perhaps the reason why no study has ever examined the capability of C. diphtheriae to use sialic acid as a nutrient in vivo, which this study would suggest it is capable of. While the identity of a sialidase Bortezomib molecular weight in C. diphtheriae has been known for

nearly 50 years, the presence of a sialidase in C. glutamicum has not been suspected. This enzyme is not orthologous to the sialidases seen in C. diphtheriae, C. ulcerans and C. pseudotuberculosis, but rather is most similar to Arthrobacter sp. The essential nature of the ABC transporter in the same gene cluster as the sialidase (cg2935) suggests that Cg2935 is a sialidase; however, this will need experimental confirmation. This study presents the first evidence for an active transporter for Neu5Ac in an actinobacterium and increases the range of bacteria that appear to use an ABC transporter for this purpose. Other bacteria where sialic acid transporters have been characterized use tripartite ATP-independent periplasmic (TRAP) transporters (Severi et al.,

2005; Mulligan et al., 2009, 2012; Chowdhury et al., 2012), classical secondary transporters of the BCKDHA major facilitator superfamily (Martinez et al., 1995; Mulligan et al., 2012) or sodium solute symporter family (SSS) transporters (Severi et al., 2010), although perhaps significantly all these are Gram-negative bacteria. The only clear work on sialic acid transport in Gram-positives are from Streptococcus pneumoniae, which also uses an ABC transporter (Marion et al., 2011a, b). The reduced growth lag when cells are precultured in the presence of sialic acid suggests either the presence of a sialic acid-specific activator or the inactivation of a repressor. Given the presence of a GntR-family transcription factor in the cluster (cg2936), it is probable that the presence of Neu5Ac or one of its catabolic product acts as the ligand to cause depression of the cluster. The additional observation is that derepression by Neu5Ac is not seen in the presence of glucose, suggesting a catabolic repression-type mechanism is in operation. The mechanisms of catabolite repression are not well studied in C. glutamicum, and in many cases, different carbon sources are co-metabolized.

diphtheriae KCTC3075 has been characterized (Kim et al., 2010), which is the orthologue of DIP0543 C. diphtheriae NCTC Navitoclax 13129 (Fig. 4), confirming that this organism has both normal sialidase but also a reported trans-sialidase activity (Mattos-Guaraldi et al., 1998). Other data suggested that C. diphtheriae harbours sialic acid on its cell envelope (Mattos-Guaraldi

et al., 1999). This could originate from the trans-sialidase activity moving sialic acid directly from host sialoglycans onto the bacterium’s surface. Both the lack of association of the sialidase with production of the diphtheria toxin (Warren & Spearing, 1963; Moriyama & Barksdale, 1967) and the lack of a need for uptake for cell surface modification were perhaps the reason why no study has ever examined the capability of C. diphtheriae to use sialic acid as a nutrient in vivo, which this study would suggest it is capable of. While the identity of a sialidase Ganetespib nmr in C. diphtheriae has been known for

nearly 50 years, the presence of a sialidase in C. glutamicum has not been suspected. This enzyme is not orthologous to the sialidases seen in C. diphtheriae, C. ulcerans and C. pseudotuberculosis, but rather is most similar to Arthrobacter sp. The essential nature of the ABC transporter in the same gene cluster as the sialidase (cg2935) suggests that Cg2935 is a sialidase; however, this will need experimental confirmation. This study presents the first evidence for an active transporter for Neu5Ac in an actinobacterium and increases the range of bacteria that appear to use an ABC transporter for this purpose. Other bacteria where sialic acid transporters have been characterized use tripartite ATP-independent periplasmic (TRAP) transporters (Severi et al.,

2005; Mulligan et al., 2009, 2012; Chowdhury et al., 2012), classical secondary transporters of the almost major facilitator superfamily (Martinez et al., 1995; Mulligan et al., 2012) or sodium solute symporter family (SSS) transporters (Severi et al., 2010), although perhaps significantly all these are Gram-negative bacteria. The only clear work on sialic acid transport in Gram-positives are from Streptococcus pneumoniae, which also uses an ABC transporter (Marion et al., 2011a, b). The reduced growth lag when cells are precultured in the presence of sialic acid suggests either the presence of a sialic acid-specific activator or the inactivation of a repressor. Given the presence of a GntR-family transcription factor in the cluster (cg2936), it is probable that the presence of Neu5Ac or one of its catabolic product acts as the ligand to cause depression of the cluster. The additional observation is that derepression by Neu5Ac is not seen in the presence of glucose, suggesting a catabolic repression-type mechanism is in operation. The mechanisms of catabolite repression are not well studied in C. glutamicum, and in many cases, different carbon sources are co-metabolized.

While MixM and many other pilotins bind the secretin subunit C-terminus, this is not always the case. The variations in secretin structure raise the issues of where the pilotin and secretin interact, and the stoichiometry of the interaction. Accessory proteins have been demonstrated to be critical in stabilizing secretins but the mechanism by which this occurs remains unknown. The stimuli that trigger secretin opening to enable passage of substrates and the role that secretins play in mediating substrate specificity selleck products also need to be determined. Structural data at the atomic level that show any of the interactions

required for secretin formation, channel dynamics, and substrate recognition would be of tremendous value not only to aid our understanding of secretin assembly but also of how large membrane-spanning complexes in general assemble and function. Following

the acceptance of this manuscript, the structure of K. oxytoca PulS was published by Tosi et al. 2011. As predicted, PulS is a Class 3 pilotin that, like E. coli GspS, contains a distinct groove formed by www.selleckchem.com/products/VX-809.html helix α1 flanked by helices α3 and α4. Mutation of the groove has shown it to be critical for PulS function. The authors would like to thank Dr. Lili Sampaleanu and Ms. Stephanie Tammam for fruitful discussions. Work in the Howell and Burrows laboratory on type IV pilus assembly is supported by grant MOP 93585 from the Canadian Institutes of Health Research (CIHR). J.K. is the recipient of a Canada Graduate scholarship from CIHR. P.L.H. and L.L.B. are recipients of a Canada Research Chair and CIHR New Investigator award, respectively. “
“Interest in probiotic bacteria, in the context of

health and disease, is increasing and gathering scientific evidence, as is reflected by their growing utilization in food and pharma PD184352 (CI-1040) industry. As a consequence, many research effort over the past few years has been dedicated to discern the molecular mechanisms responsible for their purported attributes. Remarkably, whereas the traditional probiotic concept assumes that bacteria must be alive during their administration to exert health-promoting effects, evidence is being accumulated that supports defined bacterial secreted molecules and/or isolated surface components mediating attributed cross talk dialogue between the host and the probiotic cells. Indeed, administration of the isolated bacterial-derived metabolites or molecules may be sufficient to promote the desired effects and may represent a promising safer alternative in inflammatory disorders. Here, we summarize the current knowledge of molecular effectors of probiotic bacteria that have been involved in mediating their effects. “
“Trichoderma species have been used widely as biocontrol agents for the suppression of soil-borne pathogens.

Differences in brain organisation underlying inter-subject differences in the percept of dichotically presented dissonance were determined with voxel-based morphometry. Behavioral results showed that diotic dissonant stimuli

were perceived as more unpleasant than dichotically presented dissonance, indicating that interactions within the cochlea modulated the valence percept during dissonance. However, the behavioral data also suggested that the dissonance percept did not depend crucially on the cochlea, but also occurred as a result of binaural integration when listening to dichotic dissonance. These results also showed buy BTK inhibitor substantial between-participant variations in the valence response to dichotic dissonance. These differences were in a voxel-based morphometry analysis related to differences in gray matter density in the inferior colliculus, which strongly substantiated a key role of the inferior colliculus in consonance/dissonance representation in humans. How the percept

of sensory dissonance arises in our auditory pathway has been debated for centuries. Helmholtz (1885/1954) introduced the term ‘roughness’ to define the aural sensation when hearing ‘harsh/sharp’ sounds. He claimed that roughness is caused by the acoustic interference of frequencies, a physical phenomenon that he termed beating. At a physiological level, beating has been argued to be related to the cochlea’s ability to resolve spectral components of the musical signal into critical GSK269962 in vivo bandwidths. These can be modeled as an

array of overlapping band-pass filters known as ‘auditory filters’ on the basilar PLEK2 membrane (Fletcher, 1940). Along this line of thought, beating (which corresponds to sensory or psychoacoustic dissonance) occurs when multiple frequency components interact within a critical bandwidth (Plomp & Levelt, 1965). More recent findings showed that beating/roughness seems to only play a minor role in the perception of consonance/dissonance and is subsidiary to the harmonicity of an interval (McDermott et al., 2010). Furthermore, neural pitch salience (equivalent to harmonicity) predicted behavioral interval/chord preferences better than other correlates of musical consonance/dissonance including acoustic periodicity, acoustic roughness/beating, and neural roughness/beating (Bidelman & Heinz, 2011). We know that a perception of consonance/dissonance can be evoked not only by properties of a single signal, such as roughness/beating. It can also be perceived when different pitches are presented separately to each ear in a dichotic fashion (e.g. Bidelman & Krishnan, 2009; McDermott et al., 2010). This suggests that a perception of consonance/dissonance must at least partly be generated centrally from information relayed from both cochleas.

Differences in brain organisation underlying inter-subject differences in the percept of dichotically presented dissonance were determined with voxel-based morphometry. Behavioral results showed that diotic dissonant stimuli

were perceived as more unpleasant than dichotically presented dissonance, indicating that interactions within the cochlea modulated the valence percept during dissonance. However, the behavioral data also suggested that the dissonance percept did not depend crucially on the cochlea, but also occurred as a result of binaural integration when listening to dichotic dissonance. These results also showed check details substantial between-participant variations in the valence response to dichotic dissonance. These differences were in a voxel-based morphometry analysis related to differences in gray matter density in the inferior colliculus, which strongly substantiated a key role of the inferior colliculus in consonance/dissonance representation in humans. How the percept

of sensory dissonance arises in our auditory pathway has been debated for centuries. Helmholtz (1885/1954) introduced the term ‘roughness’ to define the aural sensation when hearing ‘harsh/sharp’ sounds. He claimed that roughness is caused by the acoustic interference of frequencies, a physical phenomenon that he termed beating. At a physiological level, beating has been argued to be related to the cochlea’s ability to resolve spectral components of the musical signal into critical Cell Cycle inhibitor bandwidths. These can be modeled as an

array of overlapping band-pass filters known as ‘auditory filters’ on the basilar Thymidylate synthase membrane (Fletcher, 1940). Along this line of thought, beating (which corresponds to sensory or psychoacoustic dissonance) occurs when multiple frequency components interact within a critical bandwidth (Plomp & Levelt, 1965). More recent findings showed that beating/roughness seems to only play a minor role in the perception of consonance/dissonance and is subsidiary to the harmonicity of an interval (McDermott et al., 2010). Furthermore, neural pitch salience (equivalent to harmonicity) predicted behavioral interval/chord preferences better than other correlates of musical consonance/dissonance including acoustic periodicity, acoustic roughness/beating, and neural roughness/beating (Bidelman & Heinz, 2011). We know that a perception of consonance/dissonance can be evoked not only by properties of a single signal, such as roughness/beating. It can also be perceived when different pitches are presented separately to each ear in a dichotic fashion (e.g. Bidelman & Krishnan, 2009; McDermott et al., 2010). This suggests that a perception of consonance/dissonance must at least partly be generated centrally from information relayed from both cochleas.