The medium was then dispensed into 200 mL amounts in 500-mL Erlenmeyer flasks, stoppered with foam plugs, and autoclaved for 20 min at 121 °C. Inoculations were made with 1 mL of stationary-phase cells grown in a stress-free medium in an aerated gyratory water bath shaker, model 76 (New Brunswick Scientific), at 26 °C at 140 r.p.m. Cells and spent fluids were isolated at various growth phases. These were subsequently utilized for enzymatic, HPLC, Western blot, and biomass studies (24 h for control and

28 h for H2O2-stressed cultures, corresponding to a similar growth phase). For growth measurements, 10 mL of bacterial cultures were utilized and solubilized protein contents were monitored by the Bradford method using the Bio-Rad Protein Assay reagent (Bradford, 1976). Pseudomonas fluorescens cells were isolated at similar growth phases and resuspended in a cell storage buffer consisting of 50 mM Tris-HCl, Venetoclax research buy 5 mM MgCl2, and 1 mM phenylmethylsulfonyl fluoride (pH 7.3). CHIR-99021 cell line The cells were lysed by sonication and then centrifuged at 3000 g for 30 min at 4 °C to remove intact bacteria. Centrifugation at 180 000 g for 3 h yielded a soluble cell-free extract (CFE) and a membrane CFE. The soluble fraction was further centrifuged at 180 000 g for 1 h to obtain a membrane-free system. The purity of these fractions was

determined by monitoring G6PDH activity for the soluble component and Complex I activity for the membrane fraction. The protein content in the soluble and membrane fractions was determined PJ34 HCl using the Bradford assay (Bradford, 1976). These CFE fractions were kept at 4 °C for up to 5 days and various enzymatic activities were monitored. Various metabolite levels were determined by HPLC. Cells and spent fluids from the control and H2O2-stressed cultures were harvested at similar growth phases. Whole cells were homogenized by sonication as described above to yield CFE and then subjected to HPLC analysis following the treatment of the CFE (2 mg protein equivalent) with 0.5% v/v of perchloric acid for 10 min on ice. The precipitate was removed by centrifugation. The supernatant was then filtered and injected into an Alliance HPLC equipped with a C18 reverse-phase column

(Synergi Hydro-RP; 4 μm; 250 × 4.6 mm, Phenomenex) operating at a flow rate of 0.7 mL min−1 at ambient temperature. This flow rate was utilized for the identification of organic acids, which were monitored at 210 nm. A mobile phase consisting of 20 mM K2HPO4 (pH 2.9) was used to separate the organic acids. All the metabolites in this study were identified using known standards and the peaks were quantified using the empower software (Waters Corporation). The HPLC was standardized using a five-point calibration before each injection protocol. Peaks were routinely spiked with known standards to confirm their identities. BN-PAGE was performed following a modified method described previously (Schagger & von Jagow, 1991; Mailloux et al., 2009a, b). Cellular fractions isolated from P.

Furthermore,

although maternal BMI, gestational age and infant birth weight were not Alectinib in vitro significant in the regressions, it is possible that these are in fact important variables that we were unable to adequately account for with our limited number of subjects. Also, because all women were ART-treated, we could not evaluate the effect of exposure to HIV vs. ART. Aldrovandi’s study [8], which showed that HIV-exposed infants who were not ART-treated had lower mtDNA levels than those with HIV and ART exposure, suggests that there is a direct HIV effect on mitochondria. This has been established in HIV-infected, ART-naïve adults who have mtDNA depletion in PBMCs [39–42]. Similarly, http://www.selleckchem.com/products/PTC124.html all mothers who were on ZDV at any time during their pregnancies were also on 3TC at the same time. Therefore, it was difficult to separate exposure to ZDV from exposure to 3TC. Neither of these, however, was significant in the multivariable regression analysis. An alternative method would have been to separate groups by ZDV exposure; however, because 70% of the

HIV-infected women were on ZDV, this approach became problematic. Our cross-sectional design also prevented us from determining the longitudinal pattern of mtDNA content and mitochondrial function in the infants as their ART exposure diminished. In addition, while we showed an increase in mtDNA content in the HIV-exposed infants, we did not evaluate absolute changes in mitochondrial number. Therefore, it is impossible to know if the increased mtDNA content was secondary to an increase in mtDNA content within each mitochondrion or if there was actually a proliferation in the absolute number of mitochondria. Also, we were unable to account for genetic factors or subtle clinical differences among subjects that may have led to some of the results, especially

the outlying values. Finally, www.selleck.co.jp/products/erastin.html the HIV-infected women only had a median time of 1.7 years since diagnosis. Many of these women may have had undiagnosed HIV infection for much longer, but it is impossible to know. However, if the time between infection and diagnosis was short, this may have limited the amount of mtDNA damage seen in this study. Nevertheless, we believe that our findings add important data to those obtained in the previous studies. Our study also highlights the need to perform larger, better controlled studies specifically evaluating both mtDNA content and function, and investigating multiple tissue types simultaneously. While the benefits of interrupting MTCT far outweigh the risks associated with mtDNA toxicity, it is nonetheless important to more thoroughly describe these effects to determine if different NRTI combinations or durations should be used in pregnant women.

In one series, all four tones were drawn from the same harmonic whereas in the other they alternated between an inharmonic and harmonic complex. The harmonic tone complex had a fundamental frequency of 100 Hz, whereas the inharmonic complex had the same fundamental frequency but with each component shifted by the same amount (Δf). A harmonic complex with a 100-Hz fundamental frequency was used as it consists of components

with frequencies around 1000 Hz, where frequency discrimination was measured in Experiment 1. Both complexes had the same harmonic envelope equal to a fundamental frequency of 100 Hz but with different TFS. In each trial, one interval, selected at random, contained the harmonic complex CP-868596 nmr and the other contained the inharmonic complex. Intervals were indicated by numbered IDH targets flashing boxes presented onscreen coincident with the presentation of the complexes. Subjects clicked with a computer mouse on the box corresponding to the interval containing the inharmonic tones. Following Moore & Sęk (2009), the duration of each complex was 200 ms and the two complexes were separated by a 300-ms interval. Feedback was given after each trial, with the selected observation period flashing either

green for correct or red for incorrect. At the start of each block, Δf was set at 50 Hz and was adapted according to response. Again following Moore & Sęk (2009), blocks were terminated following eight reversals, and the threshold for the block was taken as the arithmetic mean of Δf for the last six reversals. To prevent subjects discriminating on place coding, all components were passed through a fixed band-pass filter set centered at 900 Hz with a width of 110 Hz rolling on at 30 dB per octave. Threshold equalizing noise, presented 15 dB below stimulus presentation level (SPL) and extending from 50 to 11 050 Hz, was used to mask components of the complexes falling outside the band-pass filter.

Following Moore & Sęk (2009), SPL for the harmonic complex was set 20 dB SPL above each subject’s 70.7% absolute threshold measured using an adaptive 2I-2AFC staircase method for 900 Hz immediately prior to each session. The sampled point of the psychometric function of absolute threshold was changed from Experiment 2A for consistency with previously established measures of TFS. To give consistent performance, subjects Amobarbital had one initial training session prior to testing where they practised the TFS task for ~45 min. There were two counterbalanced TFS testing sessions after training where either anodal or sham tDCS was applied, separated by a week to avoid any carry-over effects of stimulation. Subjects completed seven threshold procedures during the 20 min of either tDCS or sham stimulation. Each staircase lasted ~2 min, varying with the subject’s response times and number of trials needed for six reversals. The threshold for that session was taken as the arithmetic mean of the seven thresholds for the session, each of which lasted approximately 35 min.

According to Buchner (1960), many hatching larvae and nymphs (e.g. Selleck BMS 354825 weevils, stink bugs) own biting mouthparts with which they feed parts of the eggshell during its burst and are thus infected with the bacteria. Larval infection of P. riparius with endosymbionts most probably takes place in the same manner. However, where exactly the endosymbiotic bacteria of P. riparius are located inside the beetles was not resolved in this work and requires further FISH investigations with the novel oligonucleotide probes developed in this study. We thank J. Piel (Kekulé Institute, University of Bonn) for the supply with the ketosynthase-specific primer

pair KS1F/KS1R, H. Rödel (Institute of Animal Physiology, University of Bayreuth) for the kind introduction in sigmaplot 9.0, R. Grotjahn (Institute of Electron Microscopy, University of Bayreuth) for numerous electron-microscopical exposures, E. Helldörfer (Institute of Animal Ecology II, University of Bayreuth) for the creation of scientific figures of Paederus beetles’ anatomy, W. Nowak and I. Nowak for

the provision of several P. riparius specimens and Harold L. Drake for provision of a LINUX-based network for arb. Financial support by the Deutsche Forschungsgemeinschaft (DFG) is gratefully acknowledged (GRAKO 678). “
“Bacteria secrete small signal molecules into the environment that induce self and neighbour gene expression. This phenomenon, termed quorum sensing, allows cooperative PARP inhibitor trial behaviours that increase the fitness of the group. The best-studied signal molecules are the N-acylhomoserine lactones (AHLs), stiripentol secreted by a growing number of bacterial species including important pathogen species such as Pseudomonas aeruginosa. These molecules have recently been proposed to have properties other than those of signalling, functioning as iron quelants or antibiotics. As the presence of an acylase capable of inactivating long-chain AHLs in Anabaena sp. PCC7120 could constitute a defence mechanism against these molecules,

in this work we analyse the effects of different AHLs varying in length and substitutions on the growth and nitrogen metabolism of the cyanobacterium Anabaena sp. PCC7120. All the AHLs tested strongly inhibited nitrogen fixation. The inhibition seems to take place at post-transcriptional level, as no effect on heterocyst differentiation or on the expression of nitrogenase was observed. Moreover, N-(3-oxodecanoyl)-l-homoserine lactone (OC10-HSL) showed a specific cytotoxic effect on this cyanobacterium in the presence of a combined nitrogen source, but the mechanism involved seems to be different from that described so far for tetramic acid derivatives of oxo-substituted AHLs. These results suggest a variety of new unexpected activities for AHLs, at least on cyanobacterial populations. The term ‘quorum sensing’ (QS) (Fuqua et al.

Methods. Selleck HIF inhibitor Once a travel case was identified, the next stool from a non-traveler (not been

outside of Canada for at least 6 months) was included and cultured on the chromID-ESBL selection media. Molecular characterization was done using polymerase chain reaction and sequencing for blaCTX-Ms, blaTEMs, blaSHVs, plasmid-mediated quinolone-resistant determinants, O25-ST131, phylogenetic groups, pulsed-field gel electrophoresis (PFGE), and multilocus sequencing typing. Results. A total of 226 individuals were included; 195 (86%) were negative, and 31 (14%) were positive for ESBL-producing E coli. Notably, travelers were 5.2 (95% CI 2.1–31.1) times more likely than non-travelers to have an ESBL-producing E coli cultured from their stool. The highest rates of ESBL positivity were associated with travel to Africa or the Indian subcontinent. Among the 31 ESBL-producing E coli isolated,

22 produced CTX-M-15, 8 produced CTX-M-14, 1 produced CTX-M-8, 12 were positive for aac(6′)-Ib-cr, and 8 belonged to clone ST131. Conclusions. Our study confirms that foreign travel, especially to the Indian subcontinent and Africa, represents a major risk for rectal colonization with CTX-M-producing E coli and contributed to the Worldwide spread of these bacteria. In Gram-negative pathogens, β-lactamase production remains

the most important www.selleckchem.com/products/ink128.html contributing factor to β-lactam resistance. The extended-spectrum β-lactamases (ESBLs) have the ability to hydrolyze and cause resistance to the cephalosporins and monobactams.1 The TEM and SHV families were the predominant types of ESBLs during the 1980s and 1990s. However, since the late 1990s CTX-M ESBL enzymes have emerged Worldwide among Enterobacteriaciae, in particular Escherichia coli, and have become the most widespread type of ESBL in the world.2 CTX-M-producing E coli are important causes of community-onset urinary tract infections, bacteremia, and intra-abdominal infections. Currently, the most widespread and prevalent type of CTX-M enzyme is CTX-M-15.3 A very interesting phenomenon Farnesyltransferase about E coli that produces CTX-M-15 was described in 2008 from researchers in France and Spain. They identified [using a technique called multilocus sequencing typing (MLST)] a sequence type (ST) named ST131 among several CTX-M-15-producing E coli isolated from countries such as Spain, France, Canada, Portugal, Switzerland, Lebanon, India, Kuwait, and Korea.4,5 These two initial studies showed that ST131 had emerged seemingly independently in different parts of the world at the same time.

The most common cause of both is varicella zoster virus (VZV). ARN typically affects healthy individuals and can be caused by herpes simplex virus in younger patients and VZV in older patients [42,43]. The clinical picture is of a rapidly progressive visual loss occurring unilaterally initially. The hallmark is a progressive full-thickness retinal necrosis with confluent lesions spreading inwards from the retinal periphery. There may be associated uveitis but this is less evident in significantly immunocompromised patients, who may experience early macular involvement with no vitritis. Papillitis may occur early and result in visual loss. Retinal haemorrhages may also be present [43–46]. Visual prognosis is poor due

to the associated complications of retinal detachment, ischaemic optic neuropathy from vascular occlusion or optic nerve inflammation and macular involvement [43,44,46]. Although vitreous sampling and analysis has a role in the diagnosis of VZV retinitis MK-2206 in vivo it is not used routinely for the monitoring of the success of therapy. However, it has been ABT-199 ic50 used in the research setting [47,48]. Treatment outcomes are often disappointing,

with patients becoming blind within weeks from macular involvement and complications such as retinal detachment. A combination of intravenous ganciclovir alone or in combination with foscarnet, and intravitreal ganciclovir/foscarnet have been used to halt the progression of retinitis; however, intravenous cidofovir is probably the drug of choice, with or without the addition of intravitreal ganciclovir or foscarnet [49,50]. “
“The aim of Edoxaban this study was to assess the incidence of hepatotoxicity in patients who had used nonnucleoside reverse transcriptase inhibitors (NNRTIs) for at least 3 years. The study group consisted of HIV-infected patients under follow-up at our clinic, who had continuously used an NNRTI-containing regimen (efavirenz or nevirapine) for at least 3 years. Patients who had used

protease inhibitors (PIs) for the same time span constituted a control group. Hepatotoxicity was graded according to the modified AIDS Clinical Trial Group grading system, using alanine aminotransferase (ALT) as a marker. One hundred and twenty-two patients on an NNRTI regimen and 54 PI-using patients were included in the analysis. The mean follow-up time was nearly 6 years. Eighteen NNRTI-using patients (14.8%) developed a clinically relevant (≥ grade II) event of hepatotoxicity during treatment; five of them (4.1%) developed severe hepatotoxicity (≥ grade III). No significant difference in the hepatotoxicity rate was seen between NNRTI- and PI-using patients (14.8 vs. 18.5%, respectively; P = 0.52) or between patients using efavirenz and nevirapine (13.8% vs. 16.7%, respectively; P = 0.51). A hepatitis C virus (HCV) coinfection was associated with an increased risk of the development of hepatotoxicity during NNRTI therapy [odds ratio (OR) 1.83; 95% confidence interval (CI) 1.33–4.

However, PMM1416 has been seen to be upregulated during both P and light stress, indicating a general stress response role for this particular protein (Coleman et al., 2006). The levels of alkaline phosphatase, PhoA, were c. 28-fold more abundant in the stressed cultures, whereas the porin PhoE was c. 50-fold more abundant (Fig. 2a). At the transcriptomic level after 48 h, the regulated levels were almost at parity (Martiny et al., 2006), suggesting the differential production of both PhoE and PhoA over extended starvation periods. Increased alkaline phosphatase activity has been measured previously for oceanic picocyanobacteria under P stress

(Moore et al., 2005; Tetu et al., 2009) and in Synechocystis sp. PCC6803 (Gan, 2006), Selleck CT99021 and so our results are in line with these observations. The structure and functioning of the MED4 photosynthetic apparatus is affected through extended P starvation (Fig. 3). Seven proteins were recognized as differentially abundant (Fig. 2b). Proteins that were less abundant than the control were those associated with chlorophyll binding and light harvesting (e.g. Pcb and CP43 within PSII). Interestingly, this observation has Hedgehog inhibitor also been identified

recently at the transcriptomic level in Synechococcus WH8102 when subjected to extended P stress (Tetu et al., 2009). PsaA, which is known to be an electron acceptor in PSI, is also less abundant as well as the plastocyanin docking protein PsaF. PsaA is also a vital part of the photosynthetic

electron transport chain (PETC), and binds almost 100 chlorophyll molecules, making it an essential light-harvesting protein Phosphatidylethanolamine N-methyltransferase in PSI (Barber, 2001), specifically as MED4 has only one copy of the pcb gene, which is associated exclusively with PSII (Fig. 3) (Rocap et al., 2003). From this, we conclude that the cell reduced its photosynthetic capabilities. This would directly reduce UV photodamage and oxidative stress from reactive oxygen species produced as a byproduct of water splitting at the oxygen-evolving complex at the base of PSII. This conclusion is supported by the observation that the known antioxidants, thioredoxin (TrxA) and thioredoxin peroxidise (tpx), are not significantly differentially abundant in the stressed phenotype (Fig. 2d). It is also clear that other essential proteins in the PETC, besides PsaF, are less abundant than the P-replete control. PsaF and ferredoxin-NADP oxidoreductase are downregulated, which strongly suggests that the cell is attempting to reduce certain reductive energy production processes, specifically NADPH generation, which in turn indicates a general metabolic slowdown. It is interesting to note that essential protein subunits of the ATP synthase complex are unaffected by long-term exposure to P deprivation, which suggests that ATP was produced normally.

The strain showed resistance to ampicillin, polymixin B, co-trimoxazole, trimethoprim, streptomycin, spectinomycin, furazolidone, tetracycline, ciprofloxacin and nalidixic acid. The sequencing of int, the SXT-specific integrase and attP attachment site indicated that it possessed a variant of SXT with trimethoprim (dfrA1), sulphamethoxazole (sul2) and streptomycin (strB) resistance genes. Its mobile nature was demonstrated see more by conjugation with rifampicin-resistant Escherichia coli. The emergence of

such an isolate should be closely monitored because it will improve our understanding of the evolution of the multidrug resistance phenotype. Vibrio cholerae, the causative agent of cholera, is still a major public health problem in many developing countries of Asia, Africa and Latin America. The emergence of resistance to multiple drugs is a serious clinical problem in the treatment and containment of the disease. The occurrence of multiple antibiotic resistance in V. cholerae is being reported with

increasing frequency (Garg et al., 2000; Ramamurthy et al., 2000; Das et al., 2005). The state of Kerala is considered as endemic to the disease cholera and outbreaks this website involving multiple drug-resistant strains have been reported (Sabeena et al., 2001). The recently isolated Inaba strains from Kerala were resistant to multiple drugs (Sabu et al., 2007). The acquisition of antibiotic resistance genes is mediated by plasmids, integrons and conjugative transposons. The SXT, a conjugative element that forms a large class of mobile genetic elements, codes for genes conferring resistance to chloramphenicol (floR), streptomycin (strA and strB), sulphamethoxazole (sul2) and trimethoprim (dfrA1 and dfr18). This element can mobilize drug resistance Cell press genes from one strain to another (Waldor et al., 1996). SXT integrates into the 5′ end of prfC, a gene found on the large V. cholerae chromosome that encodes peptide chain release factor 3. The

SXT integrates into the chromosome through a recA-independent process involving site-specific recombination between a 17-bp nearly identical element (attP) and chromosomal sequences (attB) (Hochhut & Waldor, 1999). SXT integration into and excision from the chromosome requires an SXT-encoded tyrosine recombinase Int, which belongs to the λ family of site-specific recombinases (Burrus et al., 2006a). The fluoroquinolones possess excellent activity against V. cholerae O1 and O139 serogroups (Yamamoto et al., 1995). The single and multiple mutations in the quinolone-resistant determining region (QRDR) of gyrA, gyrB, parC and parE genes and overexpression of efflux pumps are associated with resistance to fluoroquinolones. In the present study, a clinical strain of V.

The PCR product was blunt-end cloned into the SmaI site of pWKS30 (Wang & Kushner, 1991) to form pYSCN. The ΔyscN mutant was made electrocompetent as previously described (Conchas & Carniel, 1990) and transformed with either vector alone or pYSCN. Transformants were selected by growth on LB Lennox agar with ampicillin (50 μg mL−1). The effect of growth on the parental, INCB018424 clinical trial ΔyscN mutant, and pLcr− strains by incubation at 37 °C with induction of the low calcium response (Straley et al., 1993) was monitored by optical density (OD620 nm). Strains were initially grown overnight at 28 °C in HI broth at 150 r.p.m. They were then diluted to an OD of approximately

0.05 in 50 mL of HI broth supplemented with either CaCl2 or MOX. The cultures were grown for 1 h at 28 °C and then elevated to 37 °C. At hourly intervals, the OD was determined. All growth curves were

performed in triplicate. Yersinia pestis strains were grown in HI broth at 28 °C for 8 h and then diluted 1/20 in HI broth containing MOX. The fresh cultures were grown for 1 h at 28 °C, switched to 37 °C, and grown overnight. The cultures were then pelleted, supernatants collected, and pellets washed. The pellets were then suspended in water with MPBio Lysing Matrix B (MP Biomedicals, Solon, 17-AAG in vitro OH), bead beat for 40 s with a FastPrep FP120 Cell Disrupter (Thermo Fisher Scientific, Pittsburg, PA), chilled on ice, bead beat again for 40 s, microfuged for 5 m, and then filtered.

The preparation was then sterility checked by plating a portion of the sample on sheep blood agar plates. The Y. pestis supernatants and uninoculated HI broth + MOX were concentrated by passage through a centrifugal filter device (Amicon Ultra-10K; Millipore, Billerica, MA), heat fixed (95 °C for 30 min), and sterility checked as described above. The protein concentrations from the samples were determined using the BCA Protein Assay Kit (Pierce, Rockford, IL) as per the manufacturer’s recommendations. Tangeritin Samples (approximately 1 μg in 2 μL) were spotted onto PVDF membrane. The membranes were blocked with 7% skim milk in PBS containing 0.1% Tween 20 (PBST). Monoclonal antibody to LcrV (DiMezzo et al., 2009) was used at a dilution of 1 : 5000 in PBST, and secondary rabbit anti-mouse horseradish peroxidase labeled antibody was used at a dilution of 1 : 5000. Reactions were visualized using 4-chloronaphthol/3,3′-diaminobenzidine (Thermo Fisher Scientific, Rockford, IL). The Y. pestis strains were prepared for mouse vaccinations or challenges as previously described (Anderson et al., 1996), except that the bacteria were suspended in 10 mM potassium phosphate buffered saline (KPBS) solution rather than HI broth. To demonstrate loss of virulence and complementation of the mutant, groups of 10 naïve female Swiss–Webster mice were challenged s.c. with CO92 wild type, ΔyscN, ΔyscN + pWKS30, or ΔyscN + pYSCN at 0.2 mL aliquots.

They also proposed that the hippocampus is critically involved in place learning and the formation and flexible utilization of cognitive maps that are independent of habitual routes

or salient cues. Although spatial cognition is a broad psychological construct that can engage multiple brain circuits, the hippocampus appears to be necessary for wayfinding (place learning), while striatal systems are critical for route learning. Moreover, this general concept of regional specialization appears to hold across mammalian species. An example from the human literature is the finding that, when humans navigate a virtual environment using a place strategy, the hippocampus is activated as assessed by neuroimaging whereas Pexidartinib ic50 when the participants use a response strategy to navigate, the caudate nucleus

is activated (Iaria et al., 2003). What happens to hippocampus-dependent behavior during aging? If rats are given the opportunity to learn a T-maze problem that can be solved equally effectively signaling pathway by using a place, response or cue strategy, each animal adopts a favored strategy to solve the problem. Probe trials can be used to test for spontaneous strategy use. When young and old rats are compared, there are no differences between age groups in number of trials to learn the task, but the predominant strategy chosen by young rats was ‘place’ whereas old rats chose ‘response’ (Barnes et al., 1980). These data indicate a shift away from hippocampus-dependent behaviors by old rats, if other solutions are equally also effective. While this observation is consistent with hippocampal dysfunction, the experiment did not test spatial learning directly. When old rats are forced to use a place strategy for optimal task performance, direct evidence is found for spatial learning and memory deficits. Examples include deficits on the Barnes maze (e.g., Barnes, 1979) and Morris watermaze (e.g., Gage et al., 1984) spatial learning and memory tasks (for review, Foster et al.,

2012). Rapp et al. (1997) have also shown spatial strategy changes in aged rhesus macaques. Advanced age also impacts navigational abilities in humans (e.g., Uttl & Graf, 1993; Burns, 1999; Driscoll et al., 2005; Moffat et al., 2006; Iaria et al., 2009; Jansen et al., 2010). For example, Head & Isom (2010) examined young and older adult performance on two different types of navigational tasks, one that required wayfinding and the other that required route learning. The virtual maze environment was identical in the two tasks. For the wayfinding task the participants were allowed to freely explore the entire environment and then, at test, were asked to find their way to a particular landmark using the shortest route. For the route-learning condition, the participants learned a specific route through the virtual environment marked by arrows and then, at test, the arrows were removed.