Steroids were continued for a median of 18 months (range 108–128

Steroids were continued for a median of 18 months (range 10.8–128.7). The combination of steroids and a second-line agent was

used in 49% (28/57) of patients at diagnosis and 79% (45/57) during the course of their illness. Sixty-three percent of patients (36/57) were treated with methotrexate (MTX) at some point in the illness and of these, 75% were commenced at diagnosis. Only 14% (4/29) of patients diagnosed prior to 2000 were managed with disease-modifying anti-rheumatic drugs (DMARDs) at diagnosis compared with 86% (24/28) of those managed after 2000 (Fig. 3). Disease course was determined in 45 (79%) patients. The remaining 12 patients had less than 36 months follow-up. The disease was monophasic in 46.7% (21/45),

Etoposide in vitro polyphasic in 17.7% (8/45) and chronic in 35.5% (16/45). For monophasic, polyphasic and chronic course, the median time to first remission was 15.7, 22 and 57.7 months, respectively. For Venetoclax the entire cohort, the median time to first remission was 22.3 months. Nine patients relapsed following a period of remission, eight with polyphasic disease and one with chronic disease. The median time to relapse for patients with polyphasic disease was 11 months (range: 8.0–20.8). Our cohort demonstrates similar epidemiological and clinical characteristics to those reported from centres in North America, South America, Japan and Europe.[1, 2, 4, 9-14] We have confirmed that female predominance, pre-pubertal

onset and a significant duration of symptoms prior to diagnosis, are common epidemiological features of this 3-mercaptopyruvate sulfurtransferase disease. We have also shown that there are a broad range of clinical features in addition to skin rash and muscle weakness which comprise the clinical syndrome of JDM. Not unexpectedly the most frequently observed clinical features at diagnosis were weakness and typical rash. Also common were myalgia, arthralgia and nailfold changes. The frequencies of these features are comparable to other studies.[1, 2, 9-11, 13-15] Calcinosis was not seen in any of our patients at diagnosis and was observed in only 18% of cases throughout the disease course. This is lower than reported rates at other centres where rates of calcinosis of up to 40% have been reported.[9-12, 14, 16, 17] The reason for the lower rates of calcinosis in the present study is unclear. It has been postulated that a longer duration of symptoms prior to diagnosis increases the risk of developing calcinosis.[10] However, the time to diagnosis in our cohort was similar to those in papers reporting higher rates of this complication. It is possible that the lower rates of calcinosis in our cohort reflect the more aggressive approach to treatment in recent years. Muscle enzymes have been reported in the literature to be abnormal in up to 90% of patients with JDM[10]; however, individual enzymes appear to be abnormal at lower rates.

“Institute of Biological, Environmental & Rural Sciences,

“Institute of Biological, Environmental & Rural Sciences, Aberystwyth University (IBERS), Aberystwyth, Ceredigion, Wales, UK Marlborough, Wiltshire, UK Concentrations of Na+, K+ and Ca2+ in the growth medium were varied within limits normally found in vivo to determine how cation concentrations affect the sensitivity of ruminal bacteria to the ionophores, monensin (a Na+/H+ and K+/H+ exchanger) and tetronasin (Ca2+/H+). High [Na+] (172 mM cf. 137 mM in control medium) enhanced the efficacy of monensin towards Eubacterium ruminantium 2388, Streptococcus Everolimus in vitro bovis C277,

Lactobacillus casei LB17 and Prevotella albensis M384. High [K+] (35 mM cf. 19 mM) alone caused a decreased potency of both ionophores, except with L. casei. Added Ca2+ (7.4

cf. 2.8 mM) increased the potency of tetronasin when [Na+] was low. High [Na+] alone also potentiated the efficacy of tetronasin. Monensin caused intracellular [Na+] and [K+] to be decreased in the most sensitive of these organisms, E. ruminantium, whereas only intracellular [Ca2+] fell with tetronasin. The changes were small; however, Δp fell by only 20 mV after 2 h when ionophores caused immediate cessation of growth. ATP concentrations fell by 77% and 75% with monensin and tetronasin, respectively. Thus, altering cation concentrations might be used to potentiate the efficacy of ionophores, by increasing the rate of energy expenditure to maintain ionic homoeostasis in sensitive bacteria. Monensin and tetronasin are feedlot ionophores that improve feed efficiency in cattle (Goodrich et al., 1984; Bartle et al., 1988). Although selleck inhibitor banned in Europe since 2006, they remain in widespread use elsewhere in the world, and research on their efficacy and mode of action continues (Dubuc et al., 2009; Felix & Loerch, 2011; Packer et al., 2011), particularly in the context of their ability to lower methane emissions

(Martin et al., 2010). Their nutritional effects are due largely to changes in the fermentation stoichiometry and the metabolism of dietary nitrogen by ruminal microorganisms (Bergen & Bates, 1984; Russell & Strobel, 1989; Duffield et al., 2012). These changes arise partly from the elimination of many next Gram-positive bacteria (Chen & Wolin, 1979; Henderson et al., 1981; Nagaraja & Taylor, 1987; Newbold et al., 1988) and partly from adaptations which resistant Gram-negative bacteria undergo when grown in the presence of ionophores (Morehead & Dawson, 1992; Newbold et al., 1992; Callaway & Russell, 1999). There has been much speculation about the molecular mode of action of feedlot ionophores, mainly by analogy with the action of ionophores on nonruminal species of bacteria (Bergen & Bates, 1984; Russell, 1987; Russell & Strobel, 1989). How ionophores affect ruminal bacteria has important implications for the possible enhancement of their potency in vivo by altering the dietary content of the cations that they translocate (Rumpler et al., 1986; Chirase et al.

Briefly, in the first survey round in 1989–1990, the entire adult

Briefly, in the first survey round in 1989–1990, the entire adult population (aged ≥13 years) of 15 neighbouring villages underwent a census and serosurvey. In 1999, 10 villages were added to the survey area. Data collection PD-0332991 mouse includes monthly recording of births and deaths, and annual house-to-house censuses and serosurveys. The Rural Clinical Cohort (RCC) presented here is nested within the GPC, and consists of a random selection of one-third of the HIV-1-seropositive adults

identified from the initial (1989–1990) survey and HIV seroconverters identified during subsequent survey rounds, together with age-stratified HIV-negative controls. Since 2004, ART-eligible GPC participants have been enrolled in the RCC to access ART, but no controls have been enrolled for these cases. Trichostatin A manufacturer RCC participants for whom there is no recorded previous negative HIV test, and for whom the date of seroconversion cannot therefore be estimated, are ‘prevalent cases’, while those for whom a date of

seroconversion can be estimated, as the midpoint of the last negative and first positive HIV tests, are ‘HIV seroconverters’. HIV seroconverters were only invited to enrol in the RCC if the interval between the last negative and first positive HIV tests was less than 4 years. Only seroconverters and HIV-negative controls were included in the present analyses. Prevalent cases were excluded from the current study. Survey staff visited the individuals identified for RCC enrolment and explained the nature of the study. Participants were invited to attend the study clinic, and, after giving written informed consent, were enrolled. They were seen every 3 months for routine appointments, at which a full medical assessment was undertaken, and were staged according to the WHO clinical staging system.

Participants were invited to visit the clinic for the investigation and treatment Cyclic nucleotide phosphodiesterase of medical problems occurring between routine appointments. All medical problems were investigated and free treatment was provided. Patients who required in-patient care were referred to the local hospital. Since 1 January 2004, free ART has been provided to eligible RCC participants, in line with the first edition of the Uganda Ministry of Health ART guidelines [13]. Individuals are eligible for ART if they have a CD4 cell count of ≤200 cells/μL, WHO clinical stage 4 disease, or advanced stage 3 disease with persistent or recurrent oral thrush and invasive bacterial infections, regardless of CD4 count, or if they are pregnant with a CD4 count of ≤250 cells/μL. First-line treatment consists of a combination of zidovudine, lamivudine and nevirapine, with the possibility of switching to stavudine in cases of zidovudine toxicity and to efavirenz in cases of nevirapine toxicity or concurrent tuberculosis. In the present study after ART initiation, participants were seen for follow-up at 2 weeks, 4 weeks and then monthly.

Converging evidence indicates that the MGE is the origin of ∼50–6

Converging evidence indicates that the MGE is the origin of ∼50–60% of the population of cortical interneurons in the mouse. In particular, the MGE gives rise to the

large majority of PV-containing and SST-containing interneurons (Fig. 3). This later group is rather heterogeneous, including cells that also contain reelin, NPY and/or CR and have distinct electrophysiological properties and morphologies (Xu et al., 2006; Miyoshi et al., 2010). Both PV- and SST-containing interneurons greatly depend on Nkx2-1 for their normal generation. The analysis of Nkx2-1 mutants selleck screening library has already revealed that this transcription factor is required for the generation of more than half of the GABAergic cells populating the cortex (Sussel et al., 1999), but it has only become clear recently that this correspond to these specific classes of interneurons. Thus, both in vitro experiments (Xu et al., 2004; Wonders et al., 2008) and in vivo transplantation analyses (Wichterle et al., 2001; Butt et al., 2005; Cobos et al., 2005; Flames et al., 2007; Wonders et al., 2008) have revealed that the majority of cortical interneurons derived from the MGE are PV-containing

(∼65%) while the remaining cells (∼35%) express SST. These studies have recently been confirmed by genetic fate-mapping studies that took advantage of the existence of genes with patterns of expression that are largely confined to the MGE, such as Nkx2-1 and Lhx6 (Fogarty et al., 2007; Xu et al., 2008), as well as by the analysis of

null or conditional mutants for these genes (Liodis Bcl-xL protein Cell press et al., 2007; Butt et al., 2008; Zhao et al., 2008). A question that remains open is to what extent progenitor cells that give rise to PV- and SST-containing interneurons are spatially segregated within the MGE. The analysis of the expression pattern of several dozens of transcription factors within the ventricular zone of the MGE has led to the proposal that this region may consist of up to five distinct progenitor domains, designated pMGE1 to pMGE5, which it has been hypothesized give rise to different classes of neurons (Flames et al., 2007). Consistently, several lines of evidence suggest that the dorsal (pMGE1-2) and ventral (pMGE3-5) regions of the MGE have a tendency to preferentially give rise to SST- and PV-containing interneurons, respectively (Flames et al., 2007; Fogarty et al., 2007; Wonders et al., 2008). Furthermore, recent fate-mapping analyses have suggested that the progenitor cells giving rise to PV-containing GABAergic neurons populating the basal ganglia might also be spatially segregated from those producing PV-containing GABAergic interneurons for the cortex (Nóbrega-Pereira et al., 2008; Flandin et al., 2010). Thus, while pMGE5 seems to originate most PV-containing GABAergic neurons in the globus pallidus, it seems to produce very few PV-containing cortical interneurons.

, 2005) Some STEC serotypes harbor a large pathogenicity island,

, 2005). Some STEC serotypes harbor a large pathogenicity island, termed the locus of enterocyte effacement (LEE), required for the formation of attaching and effacing (A/E) lesions (McDaniel & Kaper, 1997). The LEE carries the eae gene encoding the adhesin intimin, responsible for the intimate adherence of the bacteria to the enterocyte and linked to cytoskeleton rearrangements. However, the presence of the LEE does not seem to be essential for full virulence, as a wide number of LEE-negative STEC strains have been associated with sporadic cases and small outbreaks of HC and HUS (reviewed in Bettelheim, 2007). Of these LEE-negative organisms, O113:H21 is one of the most

commonly isolated STEC serotypes in many regions. Clinical isolates of LEE-negative STEC typically express Stx2 and also harbor a c. 90-kb plasmid encoding several virulence factors, including find more EHEC hemolysin (Newton et al., 2009). Some studies have elucidated different mechanisms by which these strains interact with the host intestinal

mucosa and induce disease: for example it has been demonstrated that STEC O113:H21 can invade tissue-cultured cells (Luck et al., 2006). Besides the knowledge that some STEC strains do not carry the LEE, very little is known about other strategies used by these pathogens to adhere to and colonize the host intestine. Analysis of the genome sequence of E. coli O157:H7 showed that several O157-specific islands contain putative fimbrial biosynthesis operons, including two regions encoding the long click here polar fimbriae (Lpf). The

Lpf loci are related at the genetic and protein level to Lpf of Salmonella enterica Thalidomide serovar Typhimurium and the latter have been shown to facilitate attachment of the bacteria to intestinal Peyer’s patches (Bäumler et al., 1996). In E. coli O157:H7, expression of the lpf operon 1 (lpf1) in an E. coli K-12 strain was linked to increased adherence to tissue-cultured cells and has been associated with the appearance of long fimbriae (Torres et al., 2002, 2004). The lpf2 operon has also been associated with adherence to epithelial cells and its expression in some pathogenic E. coli strains is believed to be important for the development of severe diarrhea (Doughty et al., 2002; Osek et al., 2003). Escherichia coli O157:H7 strains harboring mutations in one or both of the lpf loci (named lpf1 and lpf2 operons) have diminished intestinal colonization abilities and persistence in several animal models of infection (Jordan et al., 2004; Newton et al., 2004; Torres et al., 2007). Further, these lpf mutant strains also displayed an altered human intestinal tissue tropism (Fitzhenry et al., 2006). Cumulative evidence indicates that homologues of the lpf genes are found in other pathogenic E. coli, Salmonella, Shigella and even in some commensal E.

Multiple outbreaks have been reported following travel to the

Multiple outbreaks have been reported following travel to the

Americas, but reports of pulmonary histoplasmosis in short-term immunocompetent travelers to Africa are rare. A biology student was referred to our unit with suspected pulmonary histoplasmosis following her return from a field trip in the Ugandan rainforest. The patient informed us that several of her multinational student colleagues on the same expedition had developed a similar illness. Using an alert in ProMED-mail and a questionnaire forwarded to each of the symptomatic students, we accumulated data on the other cases involved in this apparent outbreak of pulmonary histoplasmosis. Thirteen of 24 students developed respiratory symptoms following the expedition. Chest X-ray appearances were often suggestive of miliary tuberculosis but in most cases a final diagnosis of histoplasmosis was made (confirmed with serology in five cases, clinically diagnosed in six, and retrospectively

suspected in two). Detailed questioning indicated that the likely source was a large hollow bat-infested tree within the rainforest. This is an unusual outbreak of histoplasmosis following short-term travel to Africa. Pulmonary histoplasmosis should always be considered in the differential diagnosis of an acute febrile respiratory illness in travelers returning from endemic find more areas or reporting activities suggesting exposure. Pulmonary histoplasmosis is caused by Histoplasma capsulatum,

a dimorphic fungus that is endemic in the Americas and parts of Asia and Africa.[1] It grows as a mold in soil enriched with bird or bat guano and human infection occurs after inhalation of the dust generated when such soil is disturbed.[2] Exposure can therefore occur during activities such as construction, renovation, demolition, excavation, and caving. Histoplasmosis has emerged as a health concern for travelers to endemic areas, particularly for those engaging Fenbendazole in recreational or occupational activities that disrupt contaminated soil. Multiple outbreaks have been reported among travelers to the Americas.[2] In contrast, there are few reports of infection occurring in immunocompetent persons after short-term travel to Africa. In this article we report an unusual outbreak of pulmonary histoplasmosis in travelers to Uganda. In September 2011, an outbreak of histoplasmosis in travelers to Uganda came to our attention when one of the cases was referred to our hospital (case 1). The patient had developed a respiratory illness following her return from a biology field trip in Uganda. This field trip undertaken by a multinational group of biology students involved researching insects and primates for 1 month in a rainforest near Fort Portal in western Uganda. Through the use of online social networks, the patient was aware that some of her colleagues on the field trip had developed a similar respiratory illness.

In this study, we have

In this study, we have ERK assay investigated the role of activity directly by measuring changes in medial nucleus of the

trapezoid body (MNTB) neurons in normal hearing mice subjected to 1-h sound stimulation. Broadband (4–12 kHz) chirps were used to activate MNTB neurons tonotopically restricted to the lateral MNTB, as confirmed by c-Fos-immunoreactivity. Following 1-h sound stimulation a substantial increase in Kv3.1b-immunoreactivity was measured in the lateral region of the MNTB, which lasted for 2 h before returning to control levels. Electrophysiological patch-clamp recordings in brainstem slices revealed an increase in high-threshold potassium currents in the lateral MNTB of sound-stimulated mice. Current-clamp and dynamic-clamp experiments

showed that MNTB cells from the sound-stimulated mice were able to maintain briefer action potentials during high-frequency firing than cells from control mice. These results provide evidence that acoustically PARP inhibition driven auditory activity can selectively regulate high-threshold potassium currents in the MNTB of normal hearing mice, likely due to an increased membrane expression of Kv3.1b channels. “
“The transition between biofilm and planktonic cells has important consequences during infection. As a model system, we have investigated uropathogenic Escherichia coli (UPEC) strain 536, which forms large biofilm aggregates when grown in iron-restricted tissue culture media. The provision Nintedanib (BIBF 1120) of both inorganic and physiological iron to the media induces dispersal. Aggregates do not disperse upon the addition of exogenous iron when cells are pretreated with either rifampicin or chloramphenicol as inhibitors

of transcription or translation, respectively. Aggregates stain with the cellulose stain Calcofluor White, can be prevented by the addition of cellulase to the growth media, and aggregates are broken down in the absence of exogenous iron when cellulase is added. An extension of this study to 12 UPEC clinical isolates identified seven that form cellulose aggregates under iron restriction, and that disperse upon the provision of iron. Consequently, we hypothesize that iron restriction stimulates the formation of cellulose aggregates, which disperse as a result of new gene expression in response to the provision of iron. An infection is a dynamic process whereby a pathogen will colonize the host, encounter and evade immune killing and acquire nutrients to proliferate. A successful pathogen is able to adapt to its changing environment, and especially to those changes that occur in response to bacterial activities and the damage caused by the pathogen. In the study of bacterial infections, it is important to be aware of the changes that may occur in the environment of the bacterial population during the progression of an infection. Prominent among these changes is the availability of iron, which is an essential nutrient as an enzyme cofactor for most bacteria (Schaible & Kaufmann, 2004).

This analysis includes follow-up data to a median date of May 200

This analysis includes follow-up data to a median date of May 2009. Patients starting nevirapine, efavirenz or lopinavir together with exactly two nucleoside/nucleotide reverse transcriptase GSI-IX nmr inhibitors (NRTIs) after 1 January 2000 were included in the analysis. Baseline was defined as either the date of first virological suppression (defined as a single viral load <500 HIV-1 RNA copies/mL) or 3 months after starting treatment,

whichever occurred later. Patients were excluded if they did not have a CD4 cell count or viral load measured in the 6 months prior to starting the new regimen or if they did not have any prospective follow-up. Treatment-experienced patients were included provided that they had not previously been exposed to any of the regimens of interest. Ethical approval for each participating centre is sought according to local regulations. Durability was measured as the rate of discontinuation of nevirapine, efavirenz or lopinavir, development of any serious non-AIDS-related adverse events, or worsening of other clinical or laboratory markers. The reasons for discontinuation were compared among the three regimens and the incidence of overall discontinuation

calculated. Time to discontinuation was determined using Kaplan–Meier methodology. Consistent with previous work [4,16] MK2206 in addition to discontinuation for any reason, analyses considered separately discontinuation because of toxicities or patient/physician choice and discontinuation because

of treatment failure. Reasons given for discontinuation were taken from patients’ notes and reported on standardized EuroSIDA follow-up forms (see forms at One reason for discontinuation per antiretroviral was collected. Discontinuation because of reported treatment failure included virological, immunological and clinical failure. Cox proportional hazards models, stratified by centre, were used to compare the risk of discontinuation among the three regimens. Patients Idelalisib chemical structure were followed until discontinuation of the main drug or their last recorded visit in EuroSIDA. Sensitivity analysis investigated discontinuation of any drug in the regimen and the durability of the three regimens in a subgroup of patients who were treatment naïve. The development of any serious non-AIDS clinical events or changes in clinical markers was compared among the three treatment groups using Poisson regression. Diagnosis of a non-AIDS clinical event was defined as the development of a non-AIDS-defining malignancy, pancreatitis, end-stage renal disease, grade III or IV hepatic encephalopathy, myocardial infarction, stroke or other cardiovascular disease. Changes in major clinical or laboratory markers were defined as developing or worsening anaemia, losing >10% of body weight at baseline, an increase in total cholesterol to >6.2 mmol/L or a decrease in high-density lipoprotein (HDL) cholesterol to <0.

The sequence identities shared by RecB and RecC from E coli with

The sequence identities shared by RecB and RecC from E. coli with AddA and AddB are, respectively, 17% and 11%. It is known that below 30% identity, alignment errors are frequent. Therefore, several regions were further optimized manually in order to generate sequence alignments consistent with the structural topology and constraints imposed to the AddAB complex structure. Particularly, we manually adjusted

the positions of insertions and deletions in order to ensure that burial positions Panobinostat concentration are kept hydrophobic and that the secondary structures are minimally broken by insertions. These optimized alignments were then used as starting points for generating models with modeller. The quality of the resulting models was assessed using verify3d (Luthy et al., 1992) or prosa2003 (Wiederstein & Sippl, 2007). The alignments between the sequences and the template profiles were then iteratively refined in order to reduce the alignment errors pinpointed by the evaluation scores. All H. pylori strains used were in the 26695 background (Tomb et al., 1997) and are listed in Supporting Information, Table S1. Plate cultures were grown at 37 °C under microaerobic conditions on a blood agar base medium supplemented with an antibiotic mix and 10% defibrillated horse blood (BAB). Plates were incubated from 24 h up to 5 days depending on the experiment or the strains

involved. To generate the corresponding mutant derivatives, the gene of interest cloned Romidepsin price into pILL570 was disrupted, leaving the 5′ and 3′ ends (300 bp) of the gene, by a cassette carrying a nonpolar kanamycin (Kn), an apramycin (Apr) or a chloramphenicol (Cm)

resistance gene (Marsin et al., 2008). DNA was introduced into H. pylori strains by natural transformation and selection after 3–5 days of growth on 20 μg mL−1 Kn, 12.5 μg mL−1 Apr or 8 μg mL−1 Cm. Allelic replacement GPX6 was verified by PCR. Double or triple mutant strains were obtained by plasmid or genomic DNA transformation of single mutant or by mixing two mutant strains together before plating the mix on double or triple selection. Experiments were performed on a minimum of two mutants obtained independently for each construction. For UV sensitivity assays, bacterial cell suspensions were serially diluted and 10 μL of each dilution was spotted on BAB plates. Cells were irradiated with 0, 15, 30, 45 and 60 J of 264-nm UV light delivering 1 J m−2 s−1. Gamma irradiation was performed using a 137Cs source delivering 30 Gy min−1. Survival was determined as the number of cells forming colonies on plates after a given irradiation divided by the number of colonies from nonirradiated cells. The intrachromosomal recombination substrate in the rdxA locus was described previously (Marsin et al., 2008). For insertion of the substrate into the recR gene, the Kndu∷Apra structure was amplified by PCR from plasmid pTZ954-Kndu-Apra.

Recipients were killed at the age of 16–118 months Frozen sect

Recipients were killed at the age of 1.6–11.8 months. Frozen sections were analysed by confocal immunohistochemistry for the donor cell label hPAP and synaptic markers. Vibratome slices were stained for hPAP, and processed for electron microscopy. Visual responses were recorded by electrophysiology from the superior colliculus (SC) in 12 rats at the age of 5.3–11.8 months. All recorded transplanted rats had restored or preserved visual responses in the SC corresponding to the transplant location in the retina, with thresholds between −2.8 and −3.4 log cd/m2. No such responses were found in age-matched S334ter-3 rats without

transplants, or in those with sham surgery. Donor cells and processes were identified in the host by light and electron microscopy. Transplant processes penetrated the inner host retina

in spite of occasional glial barriers between transplant and host. Labeled neuronal processes Selleck Apitolisib were found in the host inner plexiform layer, and formed apparent synapses with unlabeled cells, presumably of host origin. In conclusion, synaptic connections between graft and host cells, together with visual responses from corresponding locations this website in the brain, support the hypothesis that functional connections develop following transplantation of retinal layers into rodent models of retinal degeneration. “
“The inter-play between changes in beta-band (14–30-Hz) cortical rhythms and attention during somatosensation NADPH-cytochrome-c2 reductase informs us about where and when relevant processes occur in the brain. As such, we investigated the effects of attention on somatosensory evoked and induced responses using vibrotactile stimulation and magnetoencephalographic recording.

Subjects received trains of vibration at 23 Hz to the right index finger while watching a movie and ignoring the somatosensory stimuli or paying attention to the stimuli to detect a change in the duration of the stimulus. The amplitude of the evoked 23-Hz steady-state response in the contralateral primary somatosensory cortex (SI) was enhanced by attention and the underlying dipole source was located 2 mm more medially, indicating top-down recruitment of additional neuronal populations for the functionally relevant stimulus. Attentional modulation of the somatosensory evoked response indicates facilitation of early processing of the tactile stimulus. Beta-band activity increased after vibration offset in the contralateral primary motor cortex (MI) [event-related synchronization (ERS)] and this increase was larger for attended than ignored stimuli. Beta-band activity decreased in the ipsilateral SI prior to stimulus offset [event-related desynchronization (ERD)] for attended stimuli only. Whereas attention modulation of the evoked response was confined to the contralateral SI, event-related changes of beta-band activity involved contralateral SI–MI and inter-hemispheric SI–SI connections.