This finding nevertheless supports the need for the vaccination of all travelers against influenza regardless of age. Pneumococcal

vaccines would also benefit older travelers based on the higher proportion of individuals >60 years of age that presented with LRTI.20 We observed that HAPE proportionate morbidity was higher in older than younger ill travelers. Also, the proportion of lower respiratory infections in travelers suffering HAPE was only 12% in older individuals and 17% in the younger group in our study. While several earlier investigations in Nepal and elsewhere concluded that older A-769662 purchase age might be protective against altitude illness,21–23 recent studies challenge these conclusions.24,25 We conclude that older travelers to high-altitude destinations presented to GeoSentinel clinics comparatively more frequently than younger travelers, and that these data were not attributable to concomitant respiratory infection. We propose that older travelers have pre-travel cardiologic assessment for high-altitude travel and strictly apply prevention measures when undergoing a high-altitude trip by progressive acclimatization to altitude and use of acetazolamide. While mosquito bites were more frequently reported in older

travelers, febrile, systemic mosquito-borne illnesses like malaria and dengue were less frequent reasons for presentation in older ill travelers. We have GNE-0877 no explanation for this paradoxical finding. Severe P falciparum malaria, selleck compound however, was comparatively more frequent in the older group, which has been observed by others.26–28 As shown in a previous GeoSentinel study, older age appeared to correlate with a higher proportionate morbidity from rickettsial infections, mainly due to spotted fever-group rickettsia.29 It has been suggested that an increased likelihood of spotted fever-group

rickettsiae may be related to the increased disposable income and leisure time required for African safari itineraries.30 Although African tick-bite fever is usually benign and self-limited, it may lead to more severe complications in older travelers.31 Prevention of arthropod bites using repellents and mosquito nets and malaria chemoprophylaxis should be reinforced regardless of age. While the lower likelihood for older travelers to present with cutaneous larva migrans and schistosomiasis may not correlate with lower absolute risks of these infections, it is nevertheless possible that this finding results from a stronger adherence by older individuals to avoiding contact with wet soil and fresh water, thus less frequently engaging in at-risk activities. Finally, the higher likelihood of travel-associated UTI, gastritis, peptic ulcer, and GERD suggests that these diseases should also be considered in older travelers receiving pre-travel advice.

1. RPS. Keeping patients safe when they transfer between care providers – getting the

medicines right. Good practice guidance for healthcare professions. 2011. 2. Duggan C, Feldman R, Hough J, Bates I. Reducing adverse prescribing discrepancies following hospital discharge. Int J Pharm Pract. 1998; 6: 77–82. Lisa Mulligan, Simon White, Alison Gifford Keele University, Staffordshire, UK This study took a qualitative approach to exploring MPharm graduates’ involvement in local public health activities and their perspectives on how their undergraduate course had prepared them for this Most participants reported regular involvement in activities including provision of advice and interventions, measurement of BMN 673 cell line physical parameters and health promotion campaigns The MPharm course was commonly reported to have prepared them by instilling confidence and understanding, but a lot of participants reported that they would have preferred more preparation and especially more experience gained through practice placements The contribution that pharmacy can make to public health has been increasingly selleck products recognized in recent years and there is increasing evidence of benefit for a range of public health pharmacy services.1 Studies have surveyed pharmacy students’ perceptions of pharmacists’ public health roles and responsibilities,1 but research exploring

UK MPharm graduates’ subsequent involvement in public health activities and their perspectives on how their undergraduate education prepared them for this appears to be lacking. As such, this study aimed

to explore these topics among MPharm graduates. A qualitative approach was adopted on the basis of being well-suited to exploring the range and depth of participants’ perspectives.2 Following institutional NADPH-cytochrome-c2 reductase ethical approval, in-depth digitally recorded telephone interviews were conducted with 22 MPharm graduates working in the UK either as pre-registration pharmacists or registered pharmacists. The sample included participants from three cohorts from one school of pharmacy who were working in a variety of primary and secondary care pharmacy environments to represent as broad a range of views as possible. Participants were recruited by email to those included on the alumni database and by posting messages on social networks such as Facebook, followed by telephone contact with those who replied. The interview guide was developed from the objectives of the study and a review of the literature. Key topics included involvement in local public health activity, barriers to such involvement and their perspectives on how their undergraduate learning experience had prepared them for public health roles in practice. Interviews were transcribed verbatim and analysed using framework analysis.

Microsoft Excel and SPSS for Windows version 19.0 were used for data entry and analysis. Descriptive statistics were used to describe the demographic nature of the sample. Univariable odds ratios (OR) and 95% confidence intervals (CI) were obtained by means of logistic regression modeling. The questionnaire was sent to 475 travel health nurses, LY2835219 ic50 of whom 317 responded; 274 finished the questionnaire completely. The 43 uncompleted questionnaires were excluded

from analysis. The overall response rate was 57.9% (274/475). The response rate of the 382 registered travel health nurses was 62.3% (238/382). The characteristics of the participants are presented in Table 1. The majority (84%) has more than 10 years of nursing experience, and 60% have more than 5 years experience as travel health nurse. Of all respondents, 238 (87%) are registered in the LCR register; and 60% work at a Public Health Service facility. A substantial number of travel health nurses provide travel health

advice frequently: 90% provide at least several per week. A total of 104 respondents (38%) give advice to 100–250 patients per month, and 57% prescribe malaria chemoprophylaxis to 10–50 patients per month. BGB324 ic50 Self-reported adherence to mandatory procedures of LCR quality criteria was good: of all respondents, 99% used LCR guidelines, and 93% always had access to a consulting physician. When they gave advice, it was checked later 93% of the time by another health care professional. Of all participants, 226 (82%) aspired to have prescriptive authority. Of these, 26% believed it would improve consultations

by making them more efficient, easier, and more customer friendly. Other reasons for the aspiration were feeling competent and/or having enough experience (18%), being already engaged in prescribing according to current national protocols (16%), feeling supported by clear national guidelines (16%), and wishing to be fully responsible and/or independent (8%). The 48 participants not aspiring to have prescriptive authority said that they felt insufficiently educated and/or capable (33%), were comfortable with current ways of providing travel care (31%), and had a preference for final responsibility at physician level (23%). The respondents were also asked whether they felt cAMP competent to prescribe, and 211 (77%) gave a positive response. Their most cited reasons included sufficient experience (26%), sufficient education or qualification (20%), support from clear national guidelines (14%), and being already engaged in prescribing according to current national protocols (10%). Of those who felt competent, 22% indicated that ongoing access to a doctor would remain important, and 14% preferred to prescribe under certain conditions like a restricted number of medicines (eg, only malaria chemoprophylaxis) or only after additional education.

For naphthalene incubations, the rates were calculated in a timeframe of 435 days without an intermediate measurement. Sediment DNA was extracted using a FastDNA Spin Kit for Soil DNA extraction kit (MP Biomedicals). Genes of interest were quantified using an Applied Biosystems StepOne thermocycler. 16S rRNA gene copy numbers of Archaea and Bacteria were determined as described previously (Takai & Horikoshi, 2000; Nadkarni et al.,

2002). The concentrations of mcrA and dsrA genes were investigated according to Nunoura et al. (2006) and Schippers & Nerretin (2006), respectively. Members of the Geobacteraceae were quantified using the method described by Holmes et al. (2002). Copy numbers Selleckchem BMS-777607 are expressed as copies cm−3 sediment. Members of the microbial community in the Zeebrugge sediment were identified by the incorporation of 16S rRNA gene sequence fragments of a clone library into an existing maximum-parsimony tree (version 102) provided by Pruesse et al. (2007). Fragments of 16S rRNA genes were obtained using the modified primer sets Ar109f (5′-ACKGCTCAGTAACACGT) and Ar912r (5′-CTCCCCCGCCAATTCCTTTA) for Archaea and 27f (5′-AGAGTTTGATCCTGGCTCAG) and 907r (5′-CCATCAATTCCTTTRAGTTT) for Bacteria (Liesack & Dunfield, 2004). Subsequently, cloning was performed using the pGEM-T vector system according to the manufacturer’s instructions (Promega). All sequencing was conducted at Seqlab Göttingen

Panobinostat (Germany). Sequences were deposited at the GenBank online database Aldehyde dehydrogenase under accession numbers HM598465–HM598629. Methanogenesis was observed in all Zeebrugge microcosms after 178 days. Without added hydrocarbons, the methanogenesis rates were 2.9, 0.8, 0.6, 0.3 or 0.8 nmol methane cm−3 day−1 for ferrihydrite, manganese dioxide, nitrate, 2 or 22 mM sulfate-amended

microcosms, respectively. The respective CO2 release rates in these controls ranged from 35.5 nmol CO2 cm−3 day−1 for ferrihydrite to 73.8 nmol CO2 cm−3 day−1 for nitrate. In microcosms containing Zeebrugge sediment with hexadecane, a significant increase of methanogenesis was observed compared with control experiments without hexadecane (Fig. 2a). Moreover, hexadecane-dependent methanogenesis rates were significantly different between microcosms with and without an added electron acceptor (Fig. 2a). Most prominently, ferrihydrite accelerated hexadecane-dependent methanogenesis to 87.3±2.3 nmol methane cm−3 day−1 compared with 37.8±6.6 nmol methane cm−3 day−1 in 2 mM sulfate incubations (natural harbor water). The increase of methanogenesis in manganese dioxide incubations to 45.9±1.9 nmol methane cm−3 day−1 was insignificant compared with 2 mM sulfate incubations (Fig. 2a). Adding 20 mM sulfate decreased methanogenesis to 2.1±1.1 nmol methane cm−3 day−1. Nitrate inhibited methanogenesis completely. However, the addition of hexadecane triggered CO2 release from the microcosms (Fig. 2a). The CO2 release rates ranged from 64.6±5.8 nmol CO2 cm−3 day−1 for 2 mM sulfate to 139.6±3.

Studies of responses to the AS03-adjuvanted influenza

A/09/H1N1 vaccines in HIV-infected patients have generated diverse results. Several studies [13-15] reported low seroprotection rates of 61% [13] to 75% [14] after one dose, increasing to 92% after a second dose [16]. In contrast, seroconversion rates of 88 to 95.3% were observed after a single dose in other studies selleck [17-19]. This may be attributable to differences in the timing of immunization during the pandemic outbreak, reflected by higher baseline or follow-up seroprotection rates. The proportion of H1N1/09-infected adults identified in European sero-epidemiological studies reached 10-to-25% [9], suggesting that the post-immunization seroprotection rate of 85.6% observed in our study was mainly

vaccine-induced. Other potential confounders include vaccine dose [20], use and type of adjuvant [21], and previous seasonal influenza immunization. The severity of HIV disease was not a determinant of antibody responses in our cohort. Given the relatively BMS-777607 cell line small proportion of HAART-treated HIV-infected patients with CD4 counts of <350 cells/μL at baseline, most European studies, including ours, do not have sufficient power to formally exclude an influence of very low CD4 cell counts on antibody responses. However, the superposition of reverse distribution curves comparing HIV-positive patients with CD4 counts Beta adrenergic receptor kinase <350 and >500/cells/μL, as presented in Figure 1b, indicates that their responses were similar. The question of whether CD4 cell counts would have affected responses to a single vaccine dose cannot be answered here because of the design of our study. Bickel et al. [16] identified a lower nadir CD4 cell count in HIV-positive patients who failed to seroconvert, which we did not observe. In our study, the type of antiretroviral agents used as part of the antiretroviral regimen had only a borderline significance: HIV-positive patients on PIs tended to have higher responses than those on an

NNRTI-based regimen without PIs. This treatment effect, however, disappeared after adjustment in the multivariate analysis. Age is also known to affect humoral influenza responses, including those to the AS03-adjuvanted influenza vaccine [22]. Age was indeed a significant titre determinant in healthy subjects, lower responses being observed already between 40 and 60 years. Surprisingly, this was not observed in HIV-infected patients, as patients aged 20–40 years did not respond better than those aged 40–60 years or those aged over 60 years (Fig. 1d). Given that our study design did not include assessment of primary responses, we cannot exclude the possibility that the second vaccine dose provided a greater benefit to patients aged over 40 years, thus masking the impact of age observed in healthy subjects.

, 1996). More recent studies have shed new light on the role of the transmembrane domains for KdpD sensing and signaling (Heermann et al., 2003b). A truncated KdpD lacking all four transmembrane domains, but retaining the Arg cluster, supported kdpFABC expression in a K+-dependent manner. Furthermore, truncated KdpD proteins that lack only two transmembrane domains or derivatives in which a linker Trametinib peptide or two transmembrane domains of PutP, the Na+/proline transporter of E. coli, replaced the missing part indicated that the transmembrane domains are not essential for sensing K+ limitation, but are important

for the correct positioning of the large N- and C-terminal cytoplasmic domains to each other (Heermann et al., 2003b). Although not important for sensing K+ limitation, there are some indications that the transmembrane domains of KdpD are involved in osmosensing. A truncated KdpD lacking TM1 and TM2 was unable to sense an increase of medium osmolarity (Heermann et al., 2003b). Furthermore, the systematic replacement of each single amino acid of selleck products TM1 revealed that amino acids of this transmembrane domain are involved in osmosensing, but not in K+ sensing (Stallkamp et al., 2002). Mutational analysis of amino acids located within TM3, TM4, and the adjacent C-terminal hydrophilic region identified a number of KdpD derivatives

that were insensitive towards the K+ signal, but sensitive towards osmotic shifts (Sugiura et al., 1994). Several investigations addressed the identification of the putative K+-binding site. Cells producing

an N-terminal truncated, soluble KdpD (KdpD/Δ1–498) were able to respond to changes of the extracellular K+ concentration (Rothenbücher et al., 2006). Moreover, amino acid replacements located within TM4 and the adjacent region resulted in K+-insensitive KdpD derivatives (Brandon et al., 2000). It is predicted that TM4 forms a long helix that extends into the cytoplasm and contains the cluster of Arg residues (Zimmann et al., 2007). Random mutagenesis of the corresponding part of the kdpD gene produced KdpD derivatives that caused K+-independent kdpFABC expression. Therefore, it is assumed that the putative K+-binding site is located adjacent to TM4 in the C-terminal domain. Because most of these KdpD derivatives also exhibited ID-8 an altered response to osmotic stress (Zimmann et al., 2007), these data indicate that this part of the protein is crucial for stimulus sensing and signal transmission. The N-terminal domain of KdpD comprises two subdomains: a KdpD domain (pfam02702) that is conserved among all KdpD homologues (Heermann et al., 2000, 2003a) and a domain (USP-OKCHK) similar to the universal stress protein family (Usp) (cd01987, pfam00582) (Heermann et al., 2009a, b). There is mounting evidence that this large cytoplasmic N-terminal input domain of KdpD (KdpD/1–395, Fig. 1) is important for fine tuning of the sensor kinase.

, 1996). More recent studies have shed new light on the role of the transmembrane domains for KdpD sensing and signaling (Heermann et al., 2003b). A truncated KdpD lacking all four transmembrane domains, but retaining the Arg cluster, supported kdpFABC expression in a K+-dependent manner. Furthermore, truncated KdpD proteins that lack only two transmembrane domains or derivatives in which a linker Apoptosis inhibitor peptide or two transmembrane domains of PutP, the Na+/proline transporter of E. coli, replaced the missing part indicated that the transmembrane domains are not essential for sensing K+ limitation, but are important

for the correct positioning of the large N- and C-terminal cytoplasmic domains to each other (Heermann et al., 2003b). Although not important for sensing K+ limitation, there are some indications that the transmembrane domains of KdpD are involved in osmosensing. A truncated KdpD lacking TM1 and TM2 was unable to sense an increase of medium osmolarity (Heermann et al., 2003b). Furthermore, the systematic replacement of each single amino acid of Alpelisib TM1 revealed that amino acids of this transmembrane domain are involved in osmosensing, but not in K+ sensing (Stallkamp et al., 2002). Mutational analysis of amino acids located within TM3, TM4, and the adjacent C-terminal hydrophilic region identified a number of KdpD derivatives

that were insensitive towards the K+ signal, but sensitive towards osmotic shifts (Sugiura et al., 1994). Several investigations addressed the identification of the putative K+-binding site. Cells producing

an N-terminal truncated, soluble KdpD (KdpD/Δ1–498) were able to respond to changes of the extracellular K+ concentration (Rothenbücher et al., 2006). Moreover, amino acid replacements located within TM4 and the adjacent region resulted in K+-insensitive KdpD derivatives (Brandon et al., 2000). It is predicted that TM4 forms a long helix that extends into the cytoplasm and contains the cluster of Arg residues (Zimmann et al., 2007). Random mutagenesis of the corresponding part of the kdpD gene produced KdpD derivatives that caused K+-independent kdpFABC expression. Therefore, it is assumed that the putative K+-binding site is located adjacent to TM4 in the C-terminal domain. Because most of these KdpD derivatives also exhibited enough an altered response to osmotic stress (Zimmann et al., 2007), these data indicate that this part of the protein is crucial for stimulus sensing and signal transmission. The N-terminal domain of KdpD comprises two subdomains: a KdpD domain (pfam02702) that is conserved among all KdpD homologues (Heermann et al., 2000, 2003a) and a domain (USP-OKCHK) similar to the universal stress protein family (Usp) (cd01987, pfam00582) (Heermann et al., 2009a, b). There is mounting evidence that this large cytoplasmic N-terminal input domain of KdpD (KdpD/1–395, Fig. 1) is important for fine tuning of the sensor kinase.

Although no insertion sequence (IS) was detected in the spegg locus of S. dysgalactiae ssp. equisimilis (GCSE) strains, a five-nucleotide deletion mutation was detected in the ORF of the spegg locus of one GCSE strain at the supposed site of IS981SC insertion, resulting in a frameshift mutation. Streptococcus dysgalactiae ssp. dysgalactiae is a Gram-positive bacterium belonging to α-hemolytic Lancefield group C streptococci (GCSD) (Vieira et al., 1998). Animals such as cows and sheep are natural reservoirs of GCSD (Woo et al., 2003). GCSD is mainly associated with mastitis, subcutaneous

cellulitis, and toxic shock-like syndrome in bovines (Chénier et al., 2008); suppurative polyarthritis in lambs; and other animal infections (Scott, 2000; Lacasta et al., 2008). GCSD occasionally causes cutaneous lesions, lower limb cellulitis, meningitis, and CP-673451 chemical structure bacteremia in humans (Bert & Lambert-Zechovsky, 1997; Woo et al., 2003; Fernández-Aceñero & Fernández-López, 2006). The first epizootic outbreak caused by α-hemolytic GCSD among cultured fish populations took place in southern Japan in 2002. The infected yellowtail (Seriola quinqueradiata) and amberjack (Seriola dumerili) exhibited a typical form of necrosis in their caudal peduncles

and high mortality rates (Nomoto et al., 2004, 2006, 2008; Abdelsalam et al., 2009b). Mortality is considered to be caused by systemic granulomatous inflammatory disease and severe septicemia (Hagiwara et al., 2009). This pathogen has been isolated from kingfish Seriola lalandi in Japan; gray mullet Mugil cephalus,

Roxadustat solubility dmso basket mullet Liza alata, and cobia Rachycentron canadum in Taiwan; hybrid red tilapia Oreochromis sp. in Indonesia; pompano Trachinotus blochii and white-spotted snapper Lutjanus stellatus in Malaysia; pompano T. blochii in China (Abdelsalam et al., 2009a, b, 2010); and Amur sturgeon Acipenser schrenckii in China (Yang & Li, 2009), indicating the increasing importance of this pathogen. In addition, Koh et al. (2009) reported that GCSD caused ascending upper limb cellulitis in humans engaged in cleaning fish and hence may be considered an emerging MRIP zoonotic agent. Despite its clinical significance, the fish GCSD genome and the genetic basis of its virulence remain unknown. Therefore, the development of a vaccine against this pathogen is hindered in aquaculture due to the lack of knowledge regarding its pathogenesis and virulence determinants. M protein (emm), superantigen, and streptolysin S genes are important virulence factors in group A Streptococcus pyogenes (GAS) and group C and G S. dysgalactiae ssp. equisimilis (GCSE and GGSE, respectively) due to the contribution of these factors to invasive infections in humans and mammals (Proft et al., 1999; Igwe et al., 2003; Woo et al., 2003; Zhao et al., 2007).

, 1997). Because oligopeptides are impermeable to biological membranes, dedicated proteins (ABC transporters) are used to secrete the oligopeptides into the growth environment where they function as input for two-component transduction systems. Once they interact with a membrane-bound APO866 supplier receptor, information is transmitted

via a series of phosphorylation events that ultimately coordinate gene expression. Staphylococcus aureus is a gram-positive human pathogen, which causes a variety of conditions ranging from relatively harmless conditions, such as styes, to those that constitute a medical emergency, such as toxic shock syndrome, which occurs when the bacteria enters the body through a cut, sore, catheter, or breathing tube. Recent emergence of S. aureus strains that are resistant to methicillin, the antibiotic of choice for staph

infections, has become a significant health problem. Staphylococcus aureus exhibits a highly complex adaptive behavior, with gene regulation that is population density, time, and environment specific. A part of this behavior is regulated by at least four two-component systems (Novick, 2003), one of which, termed the agr system, uses a modified octapeptide in signaling (Ji et al., 1995). Since its identification, several genes homologous to those involved in agr signaling have been identified in pathogens including Listeria monocytogenes (Autret et al., 2003), Staphylococcus saprophyticus (Sakinc et al., 2006) and Clostridium perfringens (Ohtani et al., 2009). Like the HLs, most the octapeptides also exhibit competitive

exclusion by inhibiting signaling Selleckchem GW-572016 in foreign strains (Ji et al., 1997). The precise reasoning for this is not well understood; however, it is hypothesized to be a mechanism by which strains can exclude each other from infection sites. Further, it has been shown that the octapeptide signal from Staphylococcus epidermidis inhibits virulence factor expression in S. aureus (Otto et al., 1999) without affecting growth. Therefore, the use of ‘inhibitory’ oligopeptides as treatment for certain gram-positive bacterial infections is a promising route, offering a directed therapeutic with, presumably, small chances of the target bacteria evolving resistance. Pseudomonas quinolone signal (PQS) was recently discovered as a novel, signaling molecule. It was surprising to find PQS, an inhibitor of DNA gyrase and topoisomerase (Pesci et al., 1999; McKnight, 2000), as a potential small-molecule signal due to its hydrophobicity. It has now been shown to have a role in cell-to-cell communication (Déziel et al., 2004) and is secreted in concentrated form via vesicular transport (Mashburn & Whiteley, 2005). This makes the signaling mechanism of P. aeruginosa unique in that it does not rely on diffusion-mediated communication of the small molecule, which remains concentrated within the exported vesicle.

Motor-evoked potentials (MEPs) were then used to determine the coil position that evoked the maximal response in the right FCR. The location and trajectory of the coil over left primary motor cortex (M1) were marked using the BrainSight™ stereotaxic software to minimize variability within and across days. Resting motor threshold (RMT) was determined for each participant as the percentage of stimulator output that elicited an MEP of

≥ 50 μV peak to peak on five out of 10 trials. The site of stimulation 5-Fluoracil chemical structure for the left PMd was marked in Brainsight™ by moving one gyrus forward from the FCR ‘hot spot’ (Boyd & Linsdell, 2009). The PMd location was confirmed as the posterior aspect of the middle frontal gyrus (Munchau et al., 2002; Fridman et al., 2004). Isolation of this area from M1 was verified using single pulses to ensure that: (i) there was no electromyographic record of muscle activity recorded over the FCR, and (ii) there were no visually apparent muscle twitches in the forearm or hand. Once confirmed, the location and trajectory of the coil were recorded using BrainSight™ to ensure the consistent stimulation of the PMd across days (Boyd & Linsdell, 2009). Five hertz stimulation consisted INCB018424 datasheet of 1200 pulses delivered in 10-s trains with an inter-train interval of 10 s. Intensity

was set to 110% RMT. 1 Hz stimulation consisted of 1200 pulses delivered in 10-s trains with an inter-train interval of 1 s and an intensity of 110% RMT. Control stimulation was delivered using a custom sham coil that looks and sounds similar to the rTMS coil but does not induce any current Morin Hydrate in the underlying cortex (Magstim Company Ltd.). The parameters of the control stimulation were counterbalanced across participants such

that six participants received control stimulation that mimicked 5 Hz stimulation and five participants received control stimulation that mimicked 1 Hz stimulation. The rTMS parameters employed have been shown to induce an after-effect of approximately 15 min (Chen et al., 2003). To ensure that there was no interference with the effects of the rTMS protocols upon consolidation of motor practice, participants were required to remain quietly seated for 15 min following the end of stimulation. Following the retention test on day 5, participants were shown ten 30-s trials of continuous target movements and asked to decide if they recognized any pattern that they performed during the practice sessions. Out of the 10 trials, three contained the ‘true’ middle sequence, i.e. the same as the repeated practice sequence, and seven were foils. Individuals were considered to have explicit awareness of the repeated sequence if they could both correctly recognize 2 of the 3 repeated sequences and properly label 5 of 7 of the foils as having not been seen before (Boyd & Linsdell, 2009). Motor performance was evaluated across practice and retention in two ways.