Sílvio Sanches Veiga for the Alexa 488 anti-mouse

immunoglobulin G. This work was supported by http://www.selleckchem.com/products/pfi-2.html Fapemig and Fundação Araucária/PPSUS (11403/192). Conflict of interest statement: The authors declare that this research was conducted in the absence of any commercial relationship that could create a potential conflict of interest. “
“Many earlier studies have demonstrated that rotaviruses, like any other enteric viruses are shed in stools and primarily Libraries transmitted through fecal-oral route, person-to-person contact and fomites [1] and [2]. There has been evidence that rotaviruses may also be transmitted to individuals through respiratory droplets [2], [3] and [4]. The human rotavirus vaccine strain, HRV mimics natural rotavirus infection, replicates in the intestine of the vaccinated infants and provides protection against future rotavirus infections [5]. Studies with the human rotavirus vaccine have demonstrated that the vaccine virus is shed in the stools of vaccinated infants, with the peak shedding observed on Day 7 after first dose (76–80% of infants after Dose 1 and 18–29% of infants after Dose 2) [6]. Due

to the shedding of infectious vaccine virus in stools, there is a theoretical possibility for vaccine virus to be transmitted to unvaccinated or naive infants—a process similar to that observed in natural wild-type rotavirus infection MEK inhibitor [7]. Such transmissions are possibly expected from any live attenuated vaccines such as oral polio vaccine [8]. The phenomenon of transmission of the rotavirus vaccine strain to unvaccinated individuals raises questions about

the safety of the vaccine and the possibility of conferring indirect protection particularly in developing country settings where the vaccine coverage might be incomplete as compared to the developed countries [9]. The current study was the first of its kind that explored the possibility of horizontal transmission of the HRV rotavirus vaccine strain from one twin who received HRV vaccine to the other twin who received placebo Liothyronine Sodium living under the same household. The immunogenicity and safety of the rotavirus vaccine in transmission cases was also assessed. This phase IIIb, randomized (1:1), placebo-controlled, double-blind study conducted at one urban site in Santo Domingo, Dominican Republic (106260/NCT00396630). Baseline data from all major pediatric hospitals and nurseries was obtained in advance. Parents were informed of the study by presentations at maternity centers, distribution of brochures in health centers and by providing information to pregnant women and new parents visiting maternity centers and vaccination sites. Pairs of healthy twins living in the same household, aged 6–14 weeks at the time of enrolment, born after a gestational period of ≥32 weeks attending local primary healthcare centers, were referred to the site and recruited by the participating physicians.

Y1R may not be necessary for the cued-expression of fear, as intra-amygdalar administration of NPY robustly decreases the expression of conditioned fear,

but these effects are not replicated by Y1R agonists and are not blocked by pretreatment with a Y1R antagonist (Fendt et al., 2009). In this particular study, Y1R knockout mice showed slight elevations in Libraries freezing behavior during fear conditioning, but did not show an enhanced phenotype upon testing for the cued-expression of fear compared to wildtype mice (Fendt et al., 2009). In addition, NPY was still capable of reducing the cued-expression of fear in these Y1R deficient mice, suggesting that the Y1R may not be involved in this phase (Fendt et al., 2009). NPY can suppress the long-term incubation of conditioned fear, while delivery of NPY prior to extinction training attenuates www.selleckchem.com/erk.html freezing and enhances retention of extinguished fear memories (Gutman and et al, 2008, Lach and de Lima, 2013 and Pickens and et al, 2009). Y1R antagonism blocks NPY-induced reductions in freezing and blockade of amygdalar Y1R leads to deficient extinction retention (Gutman and et al, 2008 and Lach and de Lima, 2013). Consistent with pharmacological studies, NPY knockout mice display accelerated acquisition of conditioned fear, excessive recall of fear, and impaired fear extinction (Verma et al.,

2012). Interestingly, deletion of the Y1R has moderately similar effects, whereas knockout NVP-BEZ235 order of the Y2R has no effect on fear (Verma et al., 2012). However, double Y1R and Y2R knockout mice exhibit a remarkably similar phenotype to NPY deficient mice, indicating that both receptor subtypes do play a role in aspects of fear conditioning (Verma et al., 2012). In an inescapable footshock paradigm, interactions between the NPY and CRF systems were evident as increased amygdalar CRFR1 and decreased Y1R mRNA were found concurrently in animals

displaying enhanced freezing time, and all of these effects were reversed in parallel following re-exposure to the footshock-paired environment (Hendriksen et al., 2012). Indirect evidence for NPY interactions with norepinephrine was obtained using auditory fear conditioning, in which centrally administered NPY and a Y1R agonist blunted fear-induced tachycardia (Tovote et al., 2004). These effects were blocked by a Y1R antagonist (Tovote et al., Sitaxentan 2004). NPY is implicated in depression-like behavior and produces antidepressant effects. For example, central administration of NPY dose-dependently reduces immobility and increases swimming time in the forced swim test (Redrobe and et al, 2005, Stogner and Holmes, 2000 and Redrobe and et al, 2002), a screening paradigm for pharmacological anti-depressant activity. Y1R agonists and Y2R antagonists also produce anti-depressant effects in forced swim (Redrobe et al., 2002), whereas Y1R antagonists block the anti-depressant effects of NPY (Redrobe et al., 2002).

In contrast to the extensive data on anogenital infection (Table 11), there are no data to date on vaccine

efficacy against oropharyngeal HPV infections. This deficit is an important consideration, since the incidence of HPV-associated oropharyngeal cancer (mostly attributable to HPV16) appears to be increasing dramatically, at least in industrialized countries [87]. It is uncertain whether a trial to specifically evaluate oropharyngeal efficacy will be conducted. The premalignant precursors of oropharyngeal cancer cannot be routinely identified, making it difficult to contemplate a trial with intraepithelial neoplasia as a surrogate endpoint [88]. Current routine HPV DNA sampling methods appear to have relatively low sensitivity for detecting oropharyngeal infections, making trials using persistent infection endpoints difficult as well. Finally, approval FRAX597 of a trial with a placebo-controlled trial might be difficult, given that the vaccines are approved for other indications in the prospective study populations. Regarding other oral lesions, it would helpful to establish a surveillance system for recurrent respiratory papillomatosis, since its frequency in infants of

Gardasil®-vaccinated women is likely to decrease. In conclusion, the profiles of the HPV VLP vaccines established in the randomized clinical trials illustrate their potential as high value public health interventions and strongly support their wide spread implementation to prevent anogenital HPV infections and their associated neoplasia. The primary focus must now be on implementation issues to maximize the rapid, effective and cost-efficient Afatinib price delivery of the vaccines to those individuals that are most likely to benefit from them. The work was partially supported by public grants from the the European Commission (7th Framework Programme grant HEALTH-F3-2010-242061, PREHDICT), from the Instituto de Salud

Carlos III (Spanish Government) (grants FIS PI10/02995, RCESP C03/09, RTICESP C03/10, RTIC RD06/0020/0095 and CIBERESP) and from the Agència de Gestió d’Ajuts Universitaris i de Recerca – Generalitat de Catalunya (Catalonian Government) (grants AGAUR 2005SGR00695 and AGAUR 2009SGR126), who had no role in data collection, analysis or interpretation of results. Disclosed potential Libraries conflicts of interest JTS: Named inventor on U.S. government-owned HPV vaccine-related patents that are licensed to Merck & Co., GlaxoSmithKline, Sanofi Pasteur and Shantha Biotechnics and is entitled to limited royalties as specified by federal law. XC: Institutional support: HPV vaccine trials and epidemiological studies sponsored by GlaxoSmithKline, Merck and Sanofi Pasteur MSD. Screening and HPV testing trials partially supported by Qiagen. Personal support: Travel grants to scientific meetings and honorarium for consultancy are occasionally granted by either GlaxoSmithKline, Merck, Sanofi Pasteur MSD.

N-glycation is a protein modification that occurs more often in, for example, antibodies [20]. Alternatively it could represent heterogeneity of VP1 due to N-terminal proteolysis. A 48-kDa VP1-VP2 dimer was observed in strain O1 Manisa but not in strains of other serotypes. This must represent a disulfide-bonded dimer since only O serotype strains contain a disulfide bond between cysteine 134 of VP1 and cysteine 130 of VP2 [14]. This is confirmed by analysis of tryptic digestion fragments. Trypsin treatment of FMDV strain

O1 Kaufbeuren results in cleavage of the VP1 C-terminus after residue 200 and cleavage in an exposed loop of Microbiology inhibitor VP1, known as the GH-loop, after residues 145 and 154 [17]. We observed cleavages at the same Libraries positions in SELDI-TOF-MS experiments of trypsin-treated FMDV O1 Manisa. We also observed a tryptic digestion fragment of 40.0 kDa corresponding to a VP1 degradation product linked to VP2. This confirms the presence of a VP1–VP2 dimer. The spectral peak corresponding to VP2 was predominantly identified based on its mass and because of its specific presence after immunocapture with FMDV specific VHHs. In trypsin digestion experiments we observed two peaks that suggested partial cleavage after VP2 residue 167 both in its single and its VP1 disulfide-bonded form. VP2 cleavage at this position is to our knowledge not observed before. The spectral learn more peak corresponding

to VP3 is more difficult to identify since it is predicted to have a mass intermediate between VP1 and VP2. Occasionally a peak of low height that could represent VP3 is detectable in SELDI-TOF-MS profiles (e.g. Fig. 2c). Furthermore, when the VP1 peaks and are absent due to trypsin treatment a peak at 24.0 kDa that could represent VP3 is visible. However, this peak has a lower height than the VP1 and VP2 peaks. This is unexpected since VP1–VP3 are present in equimolar amounts in FMDV particles [1]. VP3 of all FMDV serotypes is known to form disulfide bonds to other VP3 molecules [1]. Peaks that could

represent multimerized VP3 are readily visible in the spectra of all three FMDV strains, which could explain the low height of the putative VP3 monomer peak. Alternatively, the low height of the putative VP3 peak could be due to less efficient ionization of VP3. We used SELDI-TOF-MS analysis for the characterization of FMDV antigen during various stages of vaccine preparation. In FMDV antigen preparations we could readily detect PEG6000 and BSA as well as many other proteins that presumably originate from the BHK-21 cells used for viral propagation. Especially the ability to detect PEG6000 could be of use since this non-protein compound is more difficult to detect by other methods. We also observed some limited proteolytic degradation of VP1 when FMDV antigen was stored at the elevated temperature of 35 °C, but not when antigens were properly stored at 4 °C.

Activity interference was also recorded in the diaries daily using Item 5 from the 12-Item Short-Form Health Survey (Ware et al 1996), a 5-point scale anchored by ‘not at all’ through to ‘extreme interference’. To ensure completeness of follow-up, data from the diaries were collected by telephone interview at weekly intervals for the first four weeks, then monthly or until recovery for the subsequent eight selleck screening library weeks (84 days in total). At

three months, a telephone exit interview was conducted at which the Neck Disability Index (Vernon and Mior 1991) was administered and pain scores were collected. Primary outcome: The primary outcome was the time taken from commencement of treatment to recovery from the episode of neck pain. The day of recovery from the episode of neck pain was defined as the first day of seven consecutive days on which the patient rated the intensity of their average daily neck pain as < 1 on the numerical rating scale from 0 to 10. Secondary outcomes: Secondary outcomes included time to recovery of normal activity as well as pain (numerical rating scale 0–10) and disability check details (Neck Disability Index scale 0–50) scores at

three months. Time to recovery of normal activity was defined as the first day of seven consecutive days in which the participant rated the degree of interference ‘not at all’. We examined 22 putative prognostic factors. Eight demographic variables were examined: age, gender, level of education, employment status, change of employment status due to neck pain, smoking habit, whether a compensation claim for neck pain had been lodged, and self-rated general health. Level of education was determined using items from the Australian Census 2001 (Trewin 2000). Employment status was determined using categories described by

Kenny et al (2000). Self-rated general health was measured using Item 1 of the 12-Item Short-Form Health Survey (SF-12). The 14 inhibitors clinical variables examined were: pain intensity on the 0–10 numerical rating scale, duration of neck pain, disability measured by the Neck Disability Index from 0 (none) to 50 (worst), the physical (PCS) and mental health (MCS) component summary scales of the SF-12, presence of concomitant symptoms (upper limb pain, headache, upper back pain, lower back pain, dizziness and nausea), past history of neck pain, previous sick leave for Levetiracetam neck pain, and use of analgesics. The clinical course of the episode of neck pain was described using Kaplan-Meier survival curves and using descriptive statistics. Prognostic factors were evaluated using separate prognostic models for recovery from the episode of neck pain and disability at 3 months. The first stage involved examination of the univariate relationship between the outcome and each prognostic variable, using Cox regression (for time to recovery), and linear regression (for disability at 3 months). Variables with significant associations (p < 0.

2b). All subjects responded against all antigens, except one who only had FHA- and PRN-specific responses. Between days 28 and 150–180 after vaccination the numbers of antigen-specific BVD 523 memory B cells had declined. Some subjects

were back to background levels, whereas others had maintained higher levels of antigen-specific memory B cells compared to day 0. One subject had maintained the level of FHA-specific memory B cells between days 28 and 150–180. No vaccine-responders were seen in the culture-negative group ( Fig. 2b) or against the Libraries control antigen TTd (data not shown). For an in-depth evaluation of the memory B-cell response two panels were included in the flow cytometric analysis. Panel I identified different memory B-cell subpopulations (activated, resting and tissue-like) and panel II identified IgG-switched memory B cells. Detection and analysis were performed for 12 subjects (4 culture positives, 4 culture negatives and 4 placebos). Not all subjects had samples available for all time points. No differences were found between the culture positives, culture negatives or placebo when antibody isotype-switch was evaluated

(IgD+/− and IgG+/−), data not shown. However, there was an increase in the culture-positive group at days 7 and 14 of the activated memory B cells, as well as the tissue-like memory B cells (fig. 3). This was not seen in the naïve and resting memory B-cell subpopulations, nor did the FcLR4 staining differ between the groups (data not shown). The number of responding subjects was insufficient crotamiton for a thorough correlation analysis. Therefore, a more general comparison of the B-cell responses detected was made. The Ixazomib order serological response (as detected by ELISA, reported in detail in Ref. [16]), the plasma blast response and the memory B-cell response were compared in all seven culture-positive subjects (Fig. 4). As expected, the cellular response had declined in blood at day 150–180, whereas the serological response was maintained. There were minor exceptions where subjects differed between their cellular and humoral responses, but in general the subjects

responded similarly in the antigen-specific responses detected by both ELISpot and ELISA. The novel, live attenuated pertussis vaccine candidate, BPZE1, was tested for the first time in man and showed to be safe and able to induce serological responses [16]. In this study, we evaluated the B-cell responses evoked by BPZE1 during the same trial. In total 48 subjects were recruited to the study. Out of the 36 subjects that received the vaccine 7 were colonized by BPZE1 and mounted a response against the vaccine-related antigens. Since it was a first-in-man study, the dosages used in this study were based on studies in mice [19]. An optimization of the doses may perhaps lead to a better vaccine take. The results obtained in this study are considered exploratory due to the novelty of the vaccine.

Animal experiments were approved by the Ethical committee of Utrecht University, and performed according to its regulations. The following antigens were used for vaccination and determination of specificity of monoclonal antibodies (mAb):

recombinant MAP Hsp 65 kD (rMAP Hsp60) and Hsp 70 kD (rMAP Hsp70). These antigens were produced as described earlier [6] and [17]. A recombinant C-terminal deletion mutant protein of the Hsp70 molecule was constructed, comprising the receptor binding part. It consisted of N-terminal amino acids 1–359 of wildtype Hsp70, had a molecular weight of approximately 45 kD and was designated RBS70. RBS70 was constructed by restriction endonuclease digestion of the original Selleck AZD8055 recombinant MAP Hsp70 pTrcHis expression vector with AflII (NE Biolabs, USA) and HindIII (Gibco-Invitrogen, the Netherlands) using 5 units of each enzyme selleckchem per μg DNA. The digested fragment was separated from the vector DNA by agarose gel (1%) electroforesis and isolated from the gel using a QIAEXII

kit (Promega, the Netherlands). The vector DNA was blunted by using T4 DNA polymerase (Fermentas, Germany) subsequently purified using a DNA cleaning kit (Zymo Research, USA), religated using T4 DNA ligase (Quick Ligation kit, NE Biolabs, USA) and purified using the DNA cleaning kit. Finally, chemically competent Top10 bacteria (Invitrogen, the Netherlands) were transformed with the vector DNA using a heat shock protocol provided by the manufacturer. Transformed bacteria were selected and protein expression and purification was performed similar to the procedure described for recombinant MAP Hsp70 [6]. In addition, the following antigens were used: recombinant M. tuberculosis Hsp70 (MTb), recombinant Escherichia coli (E. coli) Hsp70 and bovine Hsc70 purified from bovine brain (generous gifts from Stressgen, Canada). Purified

protein derivatives (PPDs) were produced at CVI (Lelystad, the Netherlands) as previously described [18], from MAP strain 3+5/C (PPDP), M. bovis (MB) strain AN5 (PPDB), and M. avium ssp. avium (MAA) strain D4 (PPDA). MAP strain ADP ribosylation factor 316F was grown at the CVI (generous gifts from D. Bakker). To define peptides for the screening of monoclonal antibodies and sera from cattle and goats the following HSP70 Genbank-derived sequences were used: Q00488 (MAP Hsp70); A0QLZ6 (MAA Hsp70); P0A5C0 (MB Hsp70); Libraries P0A5B9 (MTb Hsp70); P04475 (E. coli Hsp70); NP776975 (Bos taurus Hsp70-1A). A first set of 124 synthetic 14-mer peptides, with an aminoterminal cysteine, a 5 amino acids (aa) shift and an overlap of 9 aa, covering the MAP Hsp70 molecule, was synthesized using the simultaneous multiple peptide synthesis (SMPS) technique described previously [19]. To enable di-sulphate binding of peptides to the solid phase ELISA plate, an amino-terminal cysteine residue was coupled to each peptide during synthesis. For primary screening peptides were pooled in 11 groups of sequential peptides.

com where they viewed the “explanation of research study” document. To qualify for the study, participants were asked if they obtained the international student visa (F1 visa) and were originally from Mainland China. After reading that document those who wanted to continue were directed to the actual survey. An identification number was assigned to each participant to maintain anonymity and confidentially. Participants who decided not to continue could quit the survey at anytime. Data was collected between June and August 2011. Since

all of the scales were 5-point scales, item-mean scores, instead of the item total scores, were calculated as the final score for each scale to make the score of each scale comparable. The range of each scale score was from 1 to 5. Data analysis

comprised two stages: (1) identification of the factors selleck that predicted PA directly, (2) exploration PI3K Inhibitor Library datasheet of the mediation effect of the predictors on PA. Binominal nested regression modeling and mediation analysis were completed in STATA 12.0 (College Station, TX, USA), with α set at p < 0.05 for all analyses. Among those who were retained for analyses (n = 649), 504 participants answered every single question leaving 145 participants (22.3%) missing at least one value. After examining the patterns of missing data, the data appeared to be missing at random (MAR). That is, missing values did not seem to be dependent on other variables. Since using list wise deletion for MAR may significantly reduce the sample size and may cause a biased estimation, the multiple imputation method was used. 30 On average participants were 27.08 ± 4.59 years of age, had a BMI of 21.96 ± 4.10 (range 17.0–32.5), aminophylline and had spent 36.53 ± 33.86 months in the U.S. Internal consistencies of the scales (Cronbach’s α values) ranged from 0.73 to 0.94 ( Table 1). From Table 2, the imputed means for each scale were close to the raw means, which provided additional evidence for the imputation approach employed. Overall, the means ranged from 2.59 to 4.19, with relatively low average scores on self-efficacy to overcome exercise barriers, but relatively high scores on positive exercise

attitude and exercise enjoyment. Though the LTEQ has been successfully used in multiple other studies, it was not used as a primary outcome variable in the current study for several reasons. First, the distribution of scores was very skewed even after imputation (i.e., skewness = 3.82 and kurtosis = 19.10). Second, the standard deviation was larger than the total mean score (i.e., mean = 49.68, SD = 69.87). Although we tried dropping outliers and combining moderate and vigorous scores, neither approach resolved the issues we encountered with this measure in this sample. Therefore, we used the binary variable of MPAR and “does not meet MPAR” as the dependent measure of PA instead. As shown in Table 2, we were not able to normalize the distribution using transformation analysis.

He concluded that “rabbits smell what they expect, not what they sniff.” More recent electrophysiological recordings in rodents have identified prestimulus anticipatory events not only in the bulb, but also in piriform cortex and orbitofrontal cortex (Kay and Freeman, 1998 and Schoenbaum and Eichenbaum, 1995), implying http://www.selleckchem.com/products/AG-014699.html that well before an odor arrives, much of the olfactory system generates a prediction about the upcoming stimulus. Finally, in human piriform cortex, attention to olfactory

content evokes baseline deviations in fMRI activity (Zelano et al., 2005), although it is unclear whether these changes merely reflect a general attentional see more gain or reflect feature-based predictive codes about specific odors. Olfactory studies in humans and other animals increasingly show that cortical representations of odor in piriform cortex are encoded as spatially distributed ensembles (Freeman, 1979, Haberly, 1985, Haberly, 2001, Hasselmo et al., 1990, Howard et al., 2009, Illig and Haberly, 2003, Kay and Stopfer, 2006, Martin et al., 2004, Spors and

Grinvald, 2002, Stettler and Axel, 2009 and Wilson and Stevenson, 2003) evolving over a time span of seconds (Rennaker et al., 2007). Therefore, on the basis of these observations, we combined an olfactory attentional search task with functional magnetic resonance imaging (fMRI) techniques and pattern-based multivariate analyses to test three Dipeptidyl peptidase hypotheses following from the predictive coding model: (1) odor-specific predictive codes in the human olfactory brain are established prior to stimulus onset and take the form of spatially distributed templates or “search images”; (2) ensemble activity patterns should evolve in space and time over the course of a trial, such that predictive coding gives way to stimulus coding from pre- to postodor onset; and (3)

a legitimate prestimulus predictive template should be able to predict olfactory behavioral performance in the post-stimulus period. Subjects participated in a simple olfactory fMRI task in which they decided whether a particular predetermined target smell was present on each trial. In target A runs, subjects determined whether odor A was present, and in target B runs, subjects determined whether odor B was present. Stimuli consisted of odor A alone (A), odor B alone (B), or a binary mixture of odors A and B (AB), resulting in six conditions: target A with stimulus A, B, or AB (A|A, A|B, A|AB), and target B with stimulus A, B, or AB (B|A, B|B, B|AB) (Figure 1). Importantly, the physical characteristics of the stimuli were identical across runs, ensuring that the only differing aspect between target A and target B runs was the attentional focus of the subject.

Inaccurate saccades within the deadline had no time out. However, monkeys had difficulty discriminating lack of reward from an inaccurate saccade and lack of reward from slow responding. Hence, the display was removed on 25%–50% of missed-deadline trials. Monkeys quickly learned that reinforcement was only available prior to this time. All patterns of results and conclusions were unchanged by these trials. Monkeys respected the response deadlines (proportion of missed deadlines: Q Accurate: 0.18, Fast: 0.16; S Accurate: 0.19, Fast: 0.13). Some sessions included only the Fast and Selleckchem Dabrafenib Accurate conditions; for that

reason, variability should be expected to be higher in the Neutral condition. We recorded neurons in FEF, located on the anterior bank of the arcuate sulcus, using tungsten microelectrodes (2–4 MΩ, FHC) referenced to a guide tube in contact with the dura. Location was verified by evoking eye movements though low-threshold (<50 μA) microstimulation. The number of electrodes lowered on a given session ranged from one to eight. Single-unit waveforms were isolated online, sampled at 40 kHz, and resorted offline (Offline Sorter; Plexon). All surgical and experimental procedures were in accordance with the National Institutes of Health Guide for the

Care and Use of Laboratory Animals and approved by the Vanderbilt Institutional Animal Care and Use Committee. BMS-754807 cell line Neurons are categorized into three major types: visual, visuomovement, next and movement. Though classification

operates along a continuum, many observations demonstrate that these populations are functionally distinct (Cohen et al., 2009; Ray et al., 2009; Gregoriou et al., 2012). Visual neurons increase discharge rates significantly immediately after array presentation but have no saccade-related modulation. Movement neurons increase discharge rate significantly before saccade initiation but have no visual response. Visuomovement neurons exhibit both periods of modulation. To classify neurons, we used activity from a memory-guided saccade task. To test for visual responses, we used t tests to compare the average activity in the interval 75–100 ms after target presentation to the activity in the 100 ms interval preceding target presentation. To test for presaccadic activity, we used t tests to compare the average activity in the 100 ms interval before saccade initiation to the activity in the interval 500–400 ms before saccade initiation. To determine when neurons responded differently to two SAT conditions or when the target as compared to distractors appeared in the RF, we computed ms-by-ms Wilcoxon rank-sum tests, evaluating the null hypothesis that target-in-RF activity was significantly different from distractor-in-RF activity. Target selection time (TST) was the first of ten successive time points significant at the p < 0.01 level. Population TST was computed using jackknifing.