Furthermore, in at least one vaccine, it is likely that the vaccine strain has an increased association

with leukocytes – the protection of poultry against fowl typhoid is based on the rough strain of Salmonella enterica serovar Gallinarum, which may have a modified tropism similar to what we showed for the rfaL and rfaC mutants of S. Enteritidis (Matiasovic ERK inhibitor library et al., 2011). In this study, we were therefore interested in determining whether attenuated mutants, which are frequently tested as live-attenuated Salmonella vaccines, may have an increased or a decreased tropism for a particular subpopulation of porcine peripheral white blood cells (WBC). The initial aim was to use this information for the future design of improved live Salmonella vaccines for the protection of animals against S. enterica infection. However, on analyzing the results, we realized that the same information might also be useful in two additional see more cases. Firstly, it can be used when selecting the most suitable S. enterica mutant as a vector for the targeted expression of heterologous antigen(s). Secondly, because S. enterica has also been used for cancer therapy (Zhao et al., 2005; Stritzker et al., 2010), modification of its preference for particular cells

may influence either

its delivery to the site of the tumor or its very interaction with tumor cells. Salmonella enterica serovar Enteritidis strain 147 spontaneously tuclazepam resistant to nalidixic acid was used in this study (Methner et al., 2004). The construction of isogenic aroA, phoP, rfaL, rfaG, rfaC and fliC mutants and the ΔSPI1-5 mutant has been described previously (Karasova et al., 2009; Rychlik et al., 2009), except for the fact that all the strains used in this study were transformed with the pFPV25.1 plasmid constitutively expressing green fluorescent protein (GFP) (Valdivia & Falkow, 1996). The strains were subcultured in Luria–Bertani (LB) broth or LB agar at 37 °C. All these procedures have been described previously (Matiasovic et al., 2011). Briefly, peripheral blood was taken from the vena jugularis of four healthy pigs that were 3 months of age. After erythrocyte lysis and washing the leukocytes twice with Dulbecco’s phosphate-buffered saline, WBC were resuspended in Hank’s balanced salt solution at a concentration of 107 cells mL−1. If necessary, porcine heat-inactivated serum (Gibco) was added to the WBC preparation to reach a 10% concentration. WBC were infected with S. Enteritidis to reach a multiplicity of infection equal to 10.

HIV-infected persons have a propensity for MRSA SSTI and a high rate of recurrent disease. The reasons for the elevated rates of MRSA infections among HIV-infected persons appear to be multifactorial, but may be

mitigated with optimized HIV control and reductions in associated risk factors. The occurrence of methicillin-resistant Staphylococcus aureus (MRSA) infections has risen dramatically in the past decade. Initially a nosocomial pathogen, MRSA is now prevalent in the community and has become the most common cause of skin and soft tissue infections (SSTIs) [1, 2]. Furthermore, a large number of healthy persons are carriers of the organism and may serve as reservoirs within the community [3]. HIV-infected persons

are at a heightened risk of MRSA infections [4-6]. To date, there are no comprehensive published reviews of the literature on MRSA colonization and infection selleck chemicals llc among HIV-infected persons during the highly active antiretroviral therapy (HAART) era. This paper provides a review of the literature and clinical management of MRSA infections among HIV-infected persons. We searched PubMed (MEDLINE) using the keywords “HIV” and “MRSA” to identify relevant references. Our search was restricted to articles published in the HAART era (January 1996 to January 2011). We also reviewed major articles on MRSA in the general population to provide comparison data. Reference lists of the articles were also examined to identify additional citations. Colonization with S. aureus is important as it precedes and increases the risk for infection [7-9]. In www.selleckchem.com/products/E7080.html a study among HIV-infected patients

colonized with MRSA at baseline, 37% developed an SSTI, whereas only 8% of those not colonized developed an SSTI HSP90 (P < 0.001) [10]. Most commonly, infection is caused by the colonizing strain [9]. Compared with the general population, HIV-infected persons are at an increased risk for MRSA colonization [9]. In the HAART era, prevalence estimates of MRSA colonization among HIV-infected persons have been ∼4% (range 0–17%) [9-18] compared with 1.5% in the general population [19]. A recent study among HIV-infected out-patients examining carriage at multiple body sites found the highest prevalence at the nares (3.3%) followed by the perigenital (1%), throat (1%) and axillae (0.2%) regions [17]. It has been reported that the addition of a groin culture for detecting MRSA carriage can increase detection by 24% [18]. Risk factors for MRSA colonization among HIV-infected persons include poor immune status (e.g. low CD4 cell count), recent exposure to antibiotics, illicit drug use, recent hospitalizations, prior MRSA colonization or infection, and chronic skin disease [9, 10, 12-14, 18, 20, 21]. The use of trimethoprim-sulfamethoxazole (TMP-SMX) appears protective against MRSA colonization [13]. Recent studies have linked high-risk sexual behaviours to MRSA colonization.

The genomic DNA of the bacteriophage BPS13 was prepared by phenol extraction (Manfioletti & Schneider, 1988). The 834-bp-long putative endolysin gene was amplified using the following see more primers: BPS13ORF194_F (5′-GATGATTCACATATGAATATCAATACA-3′) and BPS13ORF194_R (5′-AACCCCGAAGGATCCTCTTAAT-3′). The

resultant polymerase chain reaction (PCR) product was digested with NdeI and BamHI, followed by ligation into the expression vector pET15b (Novagen, Germany) containing a His-Tag at the N-terminus. Plasmid-expressing E. coli BL21 Star™ (DE3) cells were grown until the optical density at 600 nm (OD600 nm) reached 0.5. Then, 1 mM isopropyl-β-d-thio-galactoside (IPTG) was added, followed by further incubation for 5 h at 30 °C. Cells were harvested, resuspended in lysis buffer (20 mM Tris–Cl, pH 8.0, and 300 mM NaCl), and lysed by sonication (Branson Ultrasonics).

After centrifugation at 15 000 g for 15 min, the supernatant was added to Ni-NTA Superflow resin (Qiagen, Germany) and gently mixed in a column for 1 h at 4 °C. The resin was washed with lysis buffer four times and eluted with elution buffer (20 mM Tris–Cl, pH 8.0, 300 mM NaCl, and 170 mM imidazole). The buffer was changed to storage buffer [20 mM Tris–Cl, pH 8.0, 300 mM NaCl, and 30% (v/v) glycerol] by dialysis, and the purified protein was stored selleck kinase inhibitor at −80 °C until use. The lytic activity of the endolysin was determined by measuring decreases in the optical density of the cell suspension after the addition of endolysin. Bacterial cells were grown to the exponential

phase, harvested, washed twice, and resuspended in 50 mM glycine (pH 9.5) to adjust the OD600 nm = 0.8–1.0, as described previously (Loessner et al., 1997). To test the lysis of Gram-negative bacteria, harvested cells were incubated with 0.1 M EDTA for 5 min prior to the washing and resuspension steps. The endolysin solution (100 μL) was added to 900 μL of cell suspension. In control samples, one hundred microliter of resuspension buffer PAK5 was added instead of the endolysin solution. Unless indicated otherwise, 5 μg of LysBPS13 was added per 1 mL reaction. The OD600 nm was measured after incubation at room temperature for 5 min, and the lytic activity was calculated using the following equation: 100 × (OD600 nm of control without enzyme − OD600 nm of reaction mixture)/OD600 nm of control without enzyme. When determining the optimal pH for endolysin activity, the following buffers were used for cell suspension instead of the glycine buffer: 0.1% (w/v) Trifluoroacetic acid (TFA) for pH 2.0; 50 mM sodium acetate for pH 4.0 and 5.0; 50 mM MES for pH 6.0; 50 mM potassium phosphate for pH 7.0; 50 mM Tris–Cl for pH 7.5, 8.0, and 8.5; 50 mM glycine for pH 9.0 and 9.5; and 50 mM CAPS for pH 10.0 and 10.5. Different temperatures (4–55 °C) were applied to test the effect of temperature on the enzymatic activity of 0.1 μg LysBPS13. When necessary, EDTA (300 mM), NaCl (0–300 mM), or detergents (0.1%) were added.

The genomic DNA of the bacteriophage BPS13 was prepared by phenol extraction (Manfioletti & Schneider, 1988). The 834-bp-long putative endolysin gene was amplified using the following Ku-0059436 nmr primers: BPS13ORF194_F (5′-GATGATTCACATATGAATATCAATACA-3′) and BPS13ORF194_R (5′-AACCCCGAAGGATCCTCTTAAT-3′). The

resultant polymerase chain reaction (PCR) product was digested with NdeI and BamHI, followed by ligation into the expression vector pET15b (Novagen, Germany) containing a His-Tag at the N-terminus. Plasmid-expressing E. coli BL21 Star™ (DE3) cells were grown until the optical density at 600 nm (OD600 nm) reached 0.5. Then, 1 mM isopropyl-β-d-thio-galactoside (IPTG) was added, followed by further incubation for 5 h at 30 °C. Cells were harvested, resuspended in lysis buffer (20 mM Tris–Cl, pH 8.0, and 300 mM NaCl), and lysed by sonication (Branson Ultrasonics).

After centrifugation at 15 000 g for 15 min, the supernatant was added to Ni-NTA Superflow resin (Qiagen, Germany) and gently mixed in a column for 1 h at 4 °C. The resin was washed with lysis buffer four times and eluted with elution buffer (20 mM Tris–Cl, pH 8.0, 300 mM NaCl, and 170 mM imidazole). The buffer was changed to storage buffer [20 mM Tris–Cl, pH 8.0, 300 mM NaCl, and 30% (v/v) glycerol] by dialysis, and the purified protein was stored NU7441 at −80 °C until use. The lytic activity of the endolysin was determined by measuring decreases in the optical density of the cell suspension after the addition of endolysin. Bacterial cells were grown to the exponential

phase, harvested, washed twice, and resuspended in 50 mM glycine (pH 9.5) to adjust the OD600 nm = 0.8–1.0, as described previously (Loessner et al., 1997). To test the lysis of Gram-negative bacteria, harvested cells were incubated with 0.1 M EDTA for 5 min prior to the washing and resuspension steps. The endolysin solution (100 μL) was added to 900 μL of cell suspension. In control samples, one hundred microliter of resuspension buffer BCKDHA was added instead of the endolysin solution. Unless indicated otherwise, 5 μg of LysBPS13 was added per 1 mL reaction. The OD600 nm was measured after incubation at room temperature for 5 min, and the lytic activity was calculated using the following equation: 100 × (OD600 nm of control without enzyme − OD600 nm of reaction mixture)/OD600 nm of control without enzyme. When determining the optimal pH for endolysin activity, the following buffers were used for cell suspension instead of the glycine buffer: 0.1% (w/v) Trifluoroacetic acid (TFA) for pH 2.0; 50 mM sodium acetate for pH 4.0 and 5.0; 50 mM MES for pH 6.0; 50 mM potassium phosphate for pH 7.0; 50 mM Tris–Cl for pH 7.5, 8.0, and 8.5; 50 mM glycine for pH 9.0 and 9.5; and 50 mM CAPS for pH 10.0 and 10.5. Different temperatures (4–55 °C) were applied to test the effect of temperature on the enzymatic activity of 0.1 μg LysBPS13. When necessary, EDTA (300 mM), NaCl (0–300 mM), or detergents (0.1%) were added.

Conclusions. Temperature variations in central Mexico influenced the rate of ETEC but not EAEC-associated diarrhea in the US visitors. This epidemiological finding could influence seasonal recommendations for the use of ETEC vaccines in Mexico. The frequency of travelers’ diarrhea (TD) among international travelers to tropical and semitropical regions of the developing world ranges from 10% to 60%. The highest rates of TD are seen in Latin America, Africa, and the Indian subcontinent.1 Worldwide infectious diarrhea rates are influenced by seasonal changes. Striking examples include Vibrio cholerae infection in Asia where the rates of infection double during the warm season.2 In Mexican children, rates of

Trichostatin A mw diarrhea are also influenced by seasonal changes with rotavirus diarrhea Omipalisib predominating in winter months.3

In the United States, pediatric diarrhea rates also vary seasonally, with viral causes of diarrhea predominating during the winter months and enteroaggregative Escherichia coli (EAEC) seen more commonly during spring time.4 The microbiology of TD in US visitors to Mexico reflects the bacterial enteropathogens identified in Mexican children with diarrhea. Most TD acquired in Mexico is due to enterotoxigenic E coli (ETEC) and EAEC.5,6 Previous studies have shown that the overall TD and TD due to ETEC are more common during summer than during winter months.7–9 In other regions of the world, investigators have also found seasonal variation in the etiology of TD; for instance in a study conducted in Morocco, Campylobacter spp. was associated with TD during winter Roflumilast months and ETEC was seen more commonly identified during the fall months. This is believed to relate to an increase in the ambient temperature and rainfall favoring the growth and spread of bacteria that contaminate food and water. These changes may further

evolve in response to current global climate changes. The aim of this study was to characterize seasonal differences in diarrheagenic E coli pathotypes as causes for TD over a 13-month period in a popular tourist destination in Mexico. This study was conducted in two language schools in Cuernavaca, Mexico during the summer–fall months (May, June, July, and August) of 2006 and winter months (January and February) of 2006 and 2007. Participants consisted of groups of newly arrived students from the United States who completed a diary that recorded the number and consistency of all stools passed and the presence of abdominal symptoms while in Mexico. Students were enrolled within 72 hours of arrival and followed during their stay in Mexico with daily clinic visits. Acute diarrhea was defined as the passage of three or more unformed stools within a 24-hour period plus one or more gastrointestinal symptoms. A stool sample was collected at the time of the diagnosis. Appropriate treatment for TD was provided.

Cells were continuously mixed with a magnetic stirrer. Fluorescence was monitored every 30 s using excitation/emission wavelengths of 575/615 nm with 5-nm slit widths. Results are shown without ERK inhibitor clinical trial subtraction of background fluorescence. Purified Nhe components were incubated 1 : 1 (v/v) with double-strength DDM (0.4 mM) or phosphate buffer, both at pH 7.2 for 15 min at 37 °C before mixing 1 : 1 (v/v) with an aqueous solution of 50 μM (2× final) 1-anilinonaphthalene-8-sulphonic acid (ANS; Fluka Chemicals). Once solutions had reached room temperature, samples were excited at 380 nm

and emission scans were read between 400 and 650 nm with 7-nm slit widths at 500 nm min−1. The Epacadostat cuvette was held at 25 °C. Scans are shown after subtraction of PBS and DDM. Tryptophan fluorescence was carried out as described previously (Lindbäck et al., 2010) using an excitation wavelength of 295 nm to selectively excite tryptophan. A Superdex 200 10/300 GL (Amersham Biosciences) column was loaded with the purified Nhe components in 50 mM Tris buffer pH 8 with 10 mM NaCl at a flow rate of 0.4 mL min−1 over 80 min at RT. Equal volumes (125 μL) of the Nhe proteins were mixed with DDM (3 mM) for 45 min at 37 °C prior to loading on to the column. Samples passed through a UV detector set at 220 nm. Samples were withdrawn at different times

for Western immunoblots against NheB. Dialysis membranes with molecular weight cut-off (MWCO) of 12–14 000 and 50 000 (Spectrum Laboratories Casein kinase 1 Inc., CA) were soaked and rinsed in 0.25 M phosphate buffer pH 6.8 with 10 mM NaCl. The NheB component alone (5 μg protein) with and without 2 mM DDM (105 μL total volume) was dialysed against 500 mL of buffer for 48 h at 4 °C with four buffer changes. An aliquot (20 μL) of each sample was examined

on Western blots. Purified NheB (2 μg) protein pre-incubated with and without DDM (3 mM) at 37 °C for 40 min was added to wells containing monolayer of Vero cells and incubated for 40 min at 37 °C. The monolayers were washed five times with physiological sodium chloride (37 °C) and then suspended in 50 μL 2× SDS–PAGE sample buffer. Twenty microlitres of each sample was applied to 12% SDS–PAGE and transferred to nitrocellulose membranes by Western immunoblotting. We used fluorescence of propidium to monitor for plasma membrane permeability. A 1 : 80 dilution of a 5-h culture supernatant of toxigenic B. cereus NVH 75/95 induced propidium uptake in both Vero cells and HT29 epithelial cell suspensions. Figure 1a shows the fluorescence of propidium in a suspension of Vero cells, which increased after a lag of approximately 300 s following exposure to NVH 75/95. The dependence on all three Nhe components was confirmed using the culture supernatant of a naturally occurring strain of B.

We suggest that CIN 2/3 (HSIL) should be managed according to UK national guidelines. Lesions less severe than CIN 2 should probably not be treated according to CIN 2/3 recommendations, as these low-grade lesions represent persistent HPV infection of the cervix rather than pre-malignancy (level of evidence Crizotinib chemical structure 2B). Women with HIV and CIN 2/3 treated by excisional procedures have a significantly higher treatment failure rate than HIV-negative women. A number of studies show such relapse is less frequent in the presence of HAART or higher CD4

cell counts or undetectable viral load. Multidisciplinary management of such women is thus recommended (GPP). We recommend that women with Selleckchem CP-868596 HIV who have invasive cervical cancer should be managed in the same way as HIV-negative women according to UK national guidelines, again within a multidisciplinary team framework (level of evidence 1B). 9 Anal cancer 9.5 Summary of guidance We recommend the examination under anaesthetic (EUA) of the anal canal and rectum with biopsy in all suspected cases (level of evidence 1D). We recommend that staging for anal cancer following EUA and biopsy includes computerized tomography (CT) of the chest, abdomen and pelvis and MRI of the pelvis in order to assess regional lymph nodes and tumour extension [2] (level of evidence 1B). We recommend that the management of HIV patients

with anal cancer is in specialized centres where there is MDT experience in order to ensure optimal outcomes [2] (level of evidence 1C). We suggest that centres caring for these patients should be able to provide high-resolution anoscopy (HRA) services

(level of evidence 2D). We recommend CRT with 5-fluorouracil and mitomycin C (level of evidence 1A). We recommend that all people living with HIV who are to be treated with CRT should start HAART (level Glycogen branching enzyme of evidence 1C) and opportunistic infection prophylaxis (level of evidence 1D). We suggest that salvage surgery may be appropriate for people living with HIV who experience loco-regional disease persistence or relapse following CRT (level of evidence 2D). We suggest that best supportive care may be more appropriate for patients with metastatic disease or local relapse following salvage surgery (level of evidence 2D). We suggest a similar approach in people living with HIV (level of evidence 2D) and advocate surveillance for AIN by HRA (level of evidence 2D). 10 Hodgkin Lymphoma (HL) 10.4.1 Recommendations We recommend for early-favourable HL: ABVD x2–4 + IFRT 20–30 Gy (level of evidence 1B). We recommend for early-unfavourable HL: ABVD x4 + IFRT 30 Gy (level of evidence 1B). We recommend for advanced-stage HL: ABVD x6–8 +/− RT (level of evidence 1B). 10.5.1 Recommendations We recommend patients should receive HAART during chemotherapy (level of evidence 1A).

Furthermore, our finding that the anterior insular cortex is involved in covert spatial attention is in line with previous

functional imaging studies showing responses associated with the allocation of covert (Eckert et al., 2009) as well as overt attention (Corbetta high throughput screening et al., 1991; Anderson et al., 1994) in this area. Yet, we could not identify a specific FOR in which covert search influenced the BOLD response in this region. Moreover, we also failed to find any eye-centred search-related BOLD responses in the SEF. The absence of a preference for eye-centred coding seems to be in line with the fact that also eye-head gaze shifts in monkeys evoked by electrical stimulation of the SEF can not be led back to a standard eye-centred coding scheme (Martinez-Trujillo et al., 2004). As mentioned in the Introduction, previous fMRI work suggested eye-centred coding of covert shifts of attention (Golomb & Kanwisher, 2011) in the IPS. Our finding of eye-centred coding in the full extent of the cortical network subserving attention shifting, including the IPS as well as the FEF, concurs with this report and further extends it. With respect to saccades, i.e. overt shifts of attention, there is compelling evidence for eye-centred coding for parietal BOLD responses associated with the generation of memory-guided saccades (Medendorp et al.,

2003) as well as with spatial selleck chemicals updating of visual responses (Merriam et al., 2003). Also, a more recent study using an fMRI repetition suppression approach provided support for eye-centred coding of saccades in the FEF and the IPS (Van Pelt et al., 2010). Unlike the two aforementioned saccade studies, a recent one by Pertzov et al. (2011) described evidence for the coexistence of different FORs for saccades in the IPS. While one patch in the IPS exhibited a modulation of BOLD activity in line with head-centred coding for saccades, others showed responses suggestive of eye-centred coding. Support for eye-centred coding Doxacurium chloride of visual

search/shifts of attention in humans also comes from a psychophysical study (Golomb et al., 2008) in which the allocation of spatial attention, guided by world-centred cues, was probed after saccades. As a matter of fact, the focus of attention, drawn to a specific location in the VF before the saccade stayed in the same eye-centred location after a subsequent saccade. Only later was an attentional benefit observable for the world-centred location. In other words, at least initially covert attention operates in an eye-centred FOR. On the other hand, hemispatial neglect, a syndrome characterized by an impairment of both covert and overt exploration of the left hemispace (Posner et al., 1984; Karnath, 1994), typically observed after lesions of right temporal but also parietal cortex (Karnath & Rorden, 2012), seems to be at odds with the notion of eye-centred coding of search.

2. Ninety-five per cent confidence intervals (CIs) were used and P-values ≤0.05 were considered to be statistically significant. All analyses were conducted using stata version SE 11.1 (StataCorp, College Station, TX). FK866 cost A total of 15 745 patients were registered at IDI between 2005 and 2009. By the end of 2009, 8833 patients were still in active follow-up. Median CD4 counts at registration increased from 66 cells/μL [interquartile range (IQR) 0, 234 cells/μL] in 2005 to 108 cells/μL (IQR 0, 426 cells/μL) in 2009.

With the exception of 2006, the annual proportion of patients who were eligible for ART (defined by a CD4 count <200 cells/μL and/or WHO stage IV) and initiated ART increased from 55.8% in 2005 to 69.2% in 2008, with a temporary decrease in 2006 (37.7%). The median time from registration to ART initiation decreased

over time [from 99 (IQR 43, 355) days in 2005 to 53 (IQR 28, 84) days in 2009], again with a temporary increase in 2006 [191 (IQR 69, 416) days]. Proportions of LFU in the first year of ART remained relatively stable at approximately 10%. A total of 7659 HIV-infected adults who started first-line ART between January 2005 and December 2009 were included in the study, of whom 4929 (64%) were women. The mean age was 37 years [standard check details deviation (SD) 9 years] and the median baseline CD4 count at ART initiation was 109 cells/μL (IQR 38, 176 cells/μL). Data

on baseline CD4 cell count were not available for 740 patients (10%). A regimen consisting of d4T+3TC+NVP was initiated in 3544 patients (46%), and 2971 (39%) started a regimen of ZDV+3TC+EFV. Characteristics of the patients included by year of ART initiation are shown in Table 1, and showed no difference over time except for initial ART Celecoxib regimen and baseline CD4 cell count. The median baseline CD4 count at ART initiation in 2005 was 82 cells/μL (IQR 24, 153 cells/μL) and increased every year to 148 cells/μL (IQR 61, 197 cells/μL) in 2008 and 139 cells/μL (IQR 62, 194 cells/μL) in 2009, except in 2006 [71 cells/μL (IQR 23, 154 cells/μL)]. The temporal trend in increasing baseline CD4 cell count was statistically significant (P < 0.001; Table 1 and Fig. 1). The 7659 patients contributed 6017 person-years of follow-up. Overall, 338 patients died in the first year after ART initiation. The overall mortality rate was 5.6/100 PYAR (95% CI 5.1–6.3 PYAR). The mortality rate fell from 6.5/100 PYAR (95% CI 5.5–7.6 PYAR) in 2005 to 3.6/100 PYAR (95% CI 2.2–5.8 PYAR) in 2009 (log-rank test for equality of survivor functions: P < 0.001) (Fig. 2). We performed Cox proportional hazards models of the association of various factors with mortality in the first year of ART (Table 2). Lower baseline CD4 cell count, male sex and older age were associated with an increased mortality risk.

Differential CS+ and CS− processing was visible after, but not before,

associative learning. These findings correspond to evidence for an N1m modulation obtained in our first auditory MultiCS conditioning study (Bröckelmann et al., 2011) and with the N1m effect reported in Kluge et al. (2011). While closer inspection of the time-course of the difference waves revealed an affect-specific modulation even in a time-interval this website extended until 150 ms post-stimulus we conclude that, regarding temporal characteristics of the emotion effect, there is a general close correspondence across the shock-conditioning and the auditory scene-conditioning study: both report highly Selleckchem Linsitinib resolving modulation of cortical processing starting 100 ms after CS onset and overlapping the N1m time-interval as a function of a tone’s acquired behavioural significance. The N1m is a major auditory sensory evoked component and sensitive to directed attention driven by current goals, task relevance or inherent physical salience.

Directed attention prioritises behaviourally relevant stimuli in the competition for limited processing resources by means of sensory gain control (Hillyard & Anllo-Vento, 1998). N1m amplitudes are increased for stimuli carrying behaviourally relevant or physically salient spatial and non-spatial features (Hillyard et al., 1973; Woldorff et al., 1993; Ozaki et al.,

2004; Fritz et al., 2007; Poghosyan & Ioannides, 2008). It has been suggested that motivated attention automatically engaged by appetitive and aversive stimuli with intrinsic or acquired significance for Carnitine palmitoyltransferase II basic motive systems (Lang et al., 1998b; Vuilleumier, 2005) might likewise mediate affect-specific processing of emotionally salient stimuli. Recent studies have stressed the similarities between directed and motivated attention in vision (Moratti et al., 2004; Ferrari et al., 2008; Steinberg et al., 2012a) and audition (Bröckelmann et al., 2011), and proposed that the same neural circuitry might be recruited in the presence of behaviourally relevant emotional and non-emotional stimuli. This view is supported by the current findings, not only in terms of temporal dynamics but also with regards to spatial characteristics of the N1m emotion effect. L2-MNP source estimations localised affect-specific processing in regions in parietotemporal and prefrontal cortex that showed substantial overlap with a distributed frontal–parietal–temporal network identified in our previous auditory MultiCS conditioning study (Bröckelmann et al., 2011) and implicated in neuroimaging studies on selective directed attention as a domain-independent neural circuitry underlying the control of auditory and visual attention (Corbetta & Shulman, 2002; Bidet-Caulet & Bertrand, 2005; Fritz et al., 2007).