All solvents, unless specified, were of analytical grade. Keratin was extracted from Australian Merino wool, 19.5▒µm fineness, by the sulphitolysis reaction, slightly modifying the extraction methods described in previous works [21,22]. Briefly, a fibre sample, withdrawn from a combed sliver and cleaned by Soxhlet extraction with petroleum ether, was washed with distilled water and conditioned at 20▒°C, 65% R.H. for 24▒h. Five grams of cleaned and conditioned fibres was cut into snippets some millimetres long, put in 100▒mL of aqueous solution containing urea (8▒M), Ibrutinib mouse metabisulphite (0.5▒M) and sodium

dodecyl-sulphate (SDS), adjusted to pH 6.5 with NaOH 5▒N under strong

mechanical shaking for 2▒h at 65▒°C using the Linitest apparatus. The Linitest consists of a water reservoir containing a rotative axle with two stainless steel vessels radially connected. The wool, immersed in the extraction solution, is put in the two vessels with some steel bails and the axle rotates at a frequency of 40±2▒rpm. The water temperature is thermostatically controlled and maintained constant during the test. The mixture was filtered with 5▒µm pore-size filter, using a peristaltic pump and dialyzed against distilled water using a cellulose tube PD98059 concentration (6500▒Da molecular cut-off) for 3 days at room temperature, changing distilled water four times a day. The keratin aqueous solution

obtained after dialysis was freeze-dried in order to obtain a keratin powder. Keratin membranes containing CER3 and CER6 in different ratios (Table 1) were prepared as described below: CER3 and CER6 were dispersed in formic acid using an ultrasound bath at the frequency of 50▒Hz for 2▒h. Successively, the keratin powder was added to the ceramides dispersion in order to obtain a solution at the keratin concentration of 5% w/w with respect to formic acid. The dissolution of keratin powder was performed under shaking for 2▒h at room temperature. Once keratin was dissolved, the solution was subjected to ultrasonic treatment for 2▒h in order to remove air bubbles. The solutions were cast in a 5×5▒cm2 polyethylene DNA Damage inhibitor mould at 50▒°C until constant weight. The mould was filled with 5, 7, and 10▒mL of solution, in order to obtain membranes having a thickness of about 60, or 140, or 180▒µm. The molecular weights of keratin powder were determined by electrophoresis SDS-PAGE. Before electrophoretic analysis, the keratin powder was dissolved in a reductive buffer of dithiothreitol/urea at pH 8.6 under nitrogen atmosphere for 4▒h. SDS-PAGE was performed according to Laemmli’s method [23] using XcellLock Mini Cell (Invitrogen, USA), on 12% polyacrilamide gels.

206, p = 0.029), and between HGF and PAI-1 (r = 0.212, p = 0.024). In the analyses of the potential to predict malignancy, the

median serum HGF and IL-8 levels in the benign group were chosen as reference values, and cut-off values were determined at 2SD above these values; 3457 pg/ml (1271 + 2186) and 59 pg/ml (23 + 36), respectively. HGF and IL-8 levels below these cut-offs were defined as normal, and levels above were defined as elevated. Of the women with carcinoma, 20 women had elevated HGF levels, and 17 women had elevated IL-8 levels. When we combined selleckchem the two markers, 30 of the 57 women with carcinoma had either elevated HGF or elevated IL-8 levels. The five-year overall survival for all women with carcinoma was 49%. In the women with early stage cancer, the five-year overall survival was 86%, and in women with advanced stage 26%. In the univariate analyses of survival, the following parameters were statistically significant: stage of disease, histological type, residual tumor volume, and serum level of CA 125 and IL-8 (Table 2). In a multivariate analysis, age, stage of disease and serum IL-8 level reached statistical significance (Table 3). A Kaplan–Meier plot of 5-year survival in cases with advanced

stage ovarian epithelial cancer related to IL-8 level can be seen in Fig. 2. In the present study we found that the serum levels of CA 125, IL-8, and PAI-1 were significantly higher in women with ovarian epithelial cancer compared to women with benign ovarian tumors. Most ovarian carcinomas are thought RG7204 in vivo to originate from the surface epithelium Cyclin-dependent kinase 3 or postovulatory inclusion cysts. Damages of the ovarian surface epithelium during ovulation lead to repair processes

that attract leukocytes, stimulate release of inflammatory cytokines and nitrous oxide, DNA repair, and tissue restructuring [20]. Repeated ovulations with following repair processes increase the risk of errors in replication, which may cause cancer development [20]. Activation of the nuclear factor κB (NF-κB), a family of signal-activated transcription factors, by proinflammatory cytokines may promote carcinogenesis, and thus represent a link between inflammation and cancer development. NF-κB activation regulates genes that promote tumor cell proliferation, survival, migration, inflammation, and angiogenesis [21]. Elevated serum IL-8 levels in women with ovarian cancer have been reported in several studies [17,[22], [23], [24] and [25]]. IL-8 is a CXC-family chemokine, promoting angiogenesis, invasion, and cancer metastasis by binding to the receptors CXCR1 and CXCR2 [25,26]. Induction of IL-8 expression is mainly mediated by NF-κB [26]. We have previously shown HGF to be a marker for ovarian epithelial cancer and an indicator of poor prognosis [5]. By binding to its receptor c-Met, HGF has been reported to enhance NF-κB DNA binding and NF-κB-dependent transcriptional activity [[27], [28] and [29]].

L’échographie est l’examen de choix, l’adénome lactant est décrit comme étant une lésion ovoïde à grand axe parallèle à la peau, bien limitée, d’échostructure hypoéchogène homogène avec renforcement postérieur [1], [5] and [7]. Parfois l’aspect échographique est moins typique, il peut s’agir de masse hétérogène, pseudo-kystique ou encore mal limitée [8]. Le doppler montre une hypervascularisation tumorale [5]. La mammographie

n’a qu’une place réduite dans le diagnostic de l’adénome lactant du fait de l’augmentation de la densité mammaire au cours de la grossesse et de la lactation [5], il s’agit également d’un examen irradiant exposant le fœtus à une dose de 0 à 4 mrad même après utilisation de tablier abdominal plombé [4]. Elle peut cependant avoir un intérêt dans les cas simulant un cancer du sein, en mettant en évidence les microcalcifications check details indétectables à l’échographie [4]. L’adénome lactant se manifeste dans l’IRM mammaire par une lésion bien limitée hypo-intense T1, contenant des septa. La masse se rehaussant rapidement après injection du Gadolinium contrairement au septa [1] and [5]. La valeur prédictive positive de la bénignité de la lésion

est de 100 % [5]. L’IRM est indiquée en cas de suspicion de lésion maligne et si la microbiopsie ne permet pas de donner un diagnostic [4]. La microbiopsie BMN 673 mouse est un outil indispensable au diagnostic, il s’agit d’un procédé micro-invasif mais qui peut exposer à certaines complications (notamment l’infection et la fistule cutanée spécifique du sein lactant) [8]. Elle permet d’asseoir le diagnostic en mettant en évidence une prolifération

de lobules séparés par de fines selleck screening library travées conjonctivo-vasculaires, les alvéoles sont comblées par un matériel protéique abondant. Les lobules sont bordés par des cellules à cytoplasme vacuolé et un noyau nucléolé. Ils sont doublés par des cellules myoépithéliales. Le diagnostic différentiel histologique se fait avec les autres adénomes mammaires contenant une double composante épithéliale prédominante et conjonctive de soutien minime comprenant les hamartomes (adénomyoépithélial), l’adénofibrome l’adénolipome, l’adénome cannalaire et l’adénome tubulaire [2] and [5]. La différence entre l’adénome lactant et les autres adénomes se fait par la présence dans le premier de transformations en rapport avec la lactation [2]. Cependant la biopsie peu parfois manquer le diagnostic dans le cas où elle intéresse la zone liquide de la tumeur. Il est préférable qu’elle soit réalisée sous contrôle échographique [1]. L’immuno-histochimie montre l’expression de la protéine S100 par les tissus mammaire lactant et plus fortement par les cellules de l’adénome lactant ainsi que la lactoferrine et l’alpha-lactalbumine. Le traitement chirurgical de l’adénome lactant consiste en une résection large de la tumeur. Cependant, pour l’adénome lactant géant, ceci peu porter un préjudice esthétique au sein.

On the other hand, the liquid contained in dental follicles can have high viscosity and contain protein. Such DC might show high SI on T1WI. We are currently investigating this matter. Therefore, in this review, the features of DC are considered to be as follows: the cystic cavities of DC show low to high SI on T1WI, markedly high SI on T2WI, and no enhancement. In addition, the borders of DC cysts show thin rim enhancement. Ameloblastomas show multilocular or unilocular radiolucency and are the second most common type of odontogenic

tumor. Although ameloblastomas are classified into various types, in this review we examine the solid/multicystic type and unicystic type which may show unilocular [1]. The solid/multicystic type of ameloblastoma often shows multilocular radiolucency; however, unilocular radiolucency is sometimes detected. The solid type is a solid tumor, and Selleckchem SB203580 the

multicystic type contains cysts of various sizes within solid tissue [1]. Radiography cannot histopathologically differentiate the two types. CT scanning might be useful for detecting the size and shape of a lesion, but even CE–CT might not be helpful for soft tissue characterization. Moreover, the main differential diagnosis of the solid/multicystic type of ameloblastoma is KCOT. However, definitive diagnosis of the solid/multicystic type cannot be made radiologically since similar radiographic features are displayed by KCOT. MR imaging might Buparlisib price provide more detailed information about soft tissue [8], [9], [16], [17] and [19]. Solid type ameloblastomas show homogeneous low SI on T1WI and homogeneous

high SI on T2WI, which indicates the presence of soft tissue, and strong enhancement, which reflects tumor angiogenesis (Fig. 2). Multicystic type ameloblastomas can be divided into solid and cystic portions on the basis of their MR signal intensities. The solid portions show low SI on T1WI, high SI on T2WI, and strong enhancement. The cystic portions show low SI on T1WI, markedly high SI on T2WI, and no enhancement (Fig. 3). The detection of solid portions on MRI is important for the diagnosis of neoplastic lesions. Five to 15% Molecular motor of all ameloblastomas belong to the unicystic type [23]. The main radiographic feature of the unicystic type is unilocular radiolucency [24]. Therefore, this type of ameloblastoma is often misdiagnosed as a KCOT or a dentigerous cyst. Their main histopathological feature is the presence of one large cystic cavity (luminal) in the center of the lesion, and two histopathological variants exist. The luminal variant is a cystic lesion lined by an ameloblastomatous epithelium. In addition, intraluminal extensions can occur. These ameloblastomatous epithelia are often thicker than normal or protrude into the cystic cavity. In the mural variant, the cyst wall is infiltrated by an ameloblastomatous epithelial tissue [25] and [26].

These substrates can modulate cell behavior,45 which suggests that matrilysin may have a central role in the process of invasion and tumor metastasis.46 PLX 4720 MMP-26 is frequently expressed in both normal cells and endometrium, placenta, and kidney, as well as in epithelial neoplasms from various anatomic sites. It shows proteolytic activity on various ECM components, including fibronectin, collagen IV, gelatin,

and fibrinogen.7 and 47 Cavalcante et al. (2008)25 evaluated the expression of MMP-7 and MMP-26 in syndromic and nonsyndromic keratocystic odontogenic tumors, and observed a strong epithelial expression in cases associated with Gorlin syndrome compared to non-syndromic cases, which may explain the more aggressive behavior of syndrome-associated KOTs. Studies were also performed on the immunohistochemical expression of these matrilysins in ameloblastomas and adenomatoid odontogenic tumors, trying to correlate with distinct tumor biologic behavior

of these pathologies. However, Freitas et al. (2009)26 found no statistically significant differences between the immunostaining of both lesions, but there was a significant staining for MMP-7 and MMP-26 in both the parenchyma and the stroma, suggesting a role in the process of remodeling and growth of these tumors. In our results, the immunostaining of MMP-7 in the parenchyma scores were 2 in 100% of cases, whereas MMP-26 showed some variability. In the stroma, we observed 100% staining of the matrilysins, buy Inhibitor Library thereby demonstrating the involvement of these proteins in the interaction between epithelial cells and stroma in the process of tumor growth and expansion.9 and 41 Besides Progesterone degrading ECM components, MMP-7 and MMP-26 are also able to activate other metalloproteinases, such as MMP-9. MMP-7 activates MMPs 2 and 9.48 and 49 MMPs 2 and 9 degrade collagen type IV, and these gelatinases are involved in processes of tumor invasion and metastasis,50 as referenced above. The positivity evidenced by metalloproteinases 1, 7, 9, and 26 in stromal cells

demonstrates that these enzymes are also produced by fibroblasts, endothelial cells, inflammatory lymphocytes, plasma cells, and neutrophils, which are also involved in the degradation of ECM. Similar results were found in ameloblastomas,22 and 24 adenomatoid odontogenic tumors (AOTs),26 and 27 and odontogenic cysts.28 Ghost cells are necessary prerequisites for the diagnosis of CCOT, though not pathognomonic of these lesions.19 There is still much controversy about the nature of these cells. Some researchers believe that they represent a normal or atypical keratinization,51 simple cellular degeneration, or a product of the abortive enamel matrix,52 or that they derive from apoptotic processes of odontogenic cells and originate from metaplastic transformation of odontogenic tumors.

In addition, the in vitro antioxidant activities of the pectic fraction and a methanolic extract were investigated. 1,1-Diphenyl-2-picryldydrazyl (DPPH ), thiobarbituric acid, butylated hydroxyanisole (BHA), 3-phenylphenol, ethylenediaminetetraacetic acid (EDTA), DEAE-Trisacryl® Plus, N-cyclohexyl-N′-(2-morpholinoethyl)carbodiimide, metho-p-toluenesulfonate, sodium borodeuteride, ascorbic acid, bovine serum albumin (BSA), deoxyribose,

l-arabinose, d-xylose, d-glucose, d-mannose, d-galactose, l-fucose, l-rhamnose, Adriamycin order d-galacturonic acid and dextran standards were purchased from Sigma–Aldrich Chemical Co. (St. Louis, MO, USA)., Methyl iodide (MeI), phenol, hydrogen peroxide (H2O2) and sulphuric acid were from Merck Co. (Darmstadt, Germany). All other chemicals used were of analytical grade. A commercial sample of guarana (P. cupana) seed powder (batch number 8656A8) was kindly supplied by Herbarium Laboratório Botânico (Paraná, Brazil), which is a herbal medicine pharmaceutical laboratory with a line of products made up of herbal medicine and nutritional supplements. To prepare the guarana PD0332991 ic50 powder, whole dried seeds of P. cupana L.) Kuntze, collected in Bahia-Brazil, were ground in a hammer mill (60 mesh

sieve-95%). The guarana powder was defatted with toluene:ethanol (2:1, v/v) in a Soxhlet extractor (48 h). Subsequently, the dried material was treated with methanol:water (4:1, v/v) under reflux for 20 min and was immediately cooled to room temperature and centrifuged. This residue (residue 1) was dried and used for polysaccharide extraction as follows. Residue 1 was used below for polysaccharide extraction according to the scheme depicted in Fig. 1. The extraction procedure was based on the work of Bochicchio, Petkowicz, Alquini, Busato,

and Reicher (2006) with some modifications. Successive extractions were performed in a mechanical blender. After each extraction, the sample was centrifuged, and the residue was subjected to the next extraction step. Each extract was concentrated and treated with ethanol (2:1 v/v) to obtain the precipitated polysaccharides, which were then washed three times with ethanol and dried under a vacuum. The residue 1 was first extracted with DMSO (2×) at 25 °C for 24 h and 120 h to produce fractions GD-I and GD-II, respectively. Residue 2 was subjected to sequential aqueous extractions at 25 °C (2×) and at 90 °C (2×) for 4 h each. Four fractions were obtained: GW-I (25 °C), GW-II (25 °C), GHW-I (90 °C), and GHW-II (90 °C). Then, alkaline extractions with 2 M (2×) then 4 M NaOH (2×) were performed at 25 °C for 120 min in the presence of NaBH4. Each extract was neutralised with aqueous 50% acetic acid, and the precipitated polysaccharides (hemicellulose A) were isolated by centrifugation. The resulting supernatants were dialysed, concentrated to a small volume and then precipitated with ethanol (2:1 v/v) to yield hemicellulose B fractions.

23 per 100,000 population during 2010.7 Meningococcal pneumonia is infrequent, is estimated to occur in <5%–15% of patients with invasive meningococcal disease, although the precise incidence is difficult to establish because of uncertainty in establishing the cause of pneumonia.2 and 3 Serogroup Y is more likely than other serogroups to be associated with pneumonia.3 Blood or pleural cultures that yield N. meningitidis establish the diagnosis with certainty. Meningococcal colonization of the nasopharyngeal mucosae is a critical initial step in

the pathogenesis of systemic MK-8776 mouse infection. Several cell surface structures have been identified that function as adhesins in attachment of meningococci to respiratory epithelial cells. After nasopharyngeal colonization, microaspiration of upper respiratory tract secretions containing N. meningitidis probably occurs, with the subsequent

development of pneumonia. Which virulence factors are operative in the production of lung infection and whether they are unique to serogroup Y meningococci are unknown. In addition, the conditions accounting for the increase in serogroup Y infections remain undefined. 2 Other authors have described a predilection of serogroup Y meningococcus for causing respiratory illness, including a large outbreak of predominantly respiratory. Smilack et al. reported a military outbreak that included 12 cases of serogroup Y meningococcal disease (SYMD) among members of an find more army combat training unit. In this series, 5 patients had meningococcemia, 5 had meningitis, and 2 presented with primary meningococcal pneumonia.4 Subsequently, a case series of SYMD was reported in a group of US Air Force recruits in 1971–1974.6 In that series, the predominant manifestation of serogroup Y disease was respiratory; 68 (77%) of 88 patients had meningococcal pneumonia, documented by transtracheal Reverse transcriptase aspirates in 94% of the cases. Only 4 (6%) of the 68 patients with pneumonia had positive blood cultures.5

Among the patients with pneumonia, the response to antibiotic therapy was prompt; 93% of the patients were afebrile within 3 days of antibiotic therapy.2 The outcome of meningococcal pneumonia when treated is generally favorable, but the diagnosis requires a high index of suspicion, testing of respiratory samples, and blood cultures. In conclusion, we report a case of bacteraemic pneumonia caused by N. meningitidis serogroup Y with reduced susceptibility to penicillin in an adult patient. All authors report no conflicts of interest relevant to this study. “
“The recent report on “Red Ginseng and H5N1 influenza infection” in this journal is very interesting [1]. Park et al [1] noted that “the diet with the immune-enhancing Red Ginseng could help humans to overcome the infections by HP H5N1 influenza virus.

The solid line in Fig. 2b represents the prediction of Eq. (3) and shows good agreement with the experimental data (open squares). This provides convincing evidence of the basic picture proposed. Fig. 5 shows how spherulite radii vary with the pH of the solution. We find the same trend for all protein concentrations. At low pH (1–1.75) the radius increases systematically with pH. It is worth noting that differences in aggregation must largely depend on either differences in colloidal

stability or sticking RG7204 ic50 probability due, for instance, to conformational changes in the protein structure. Colloidal stability is determined by the DLVO potential surrounding each protein. This is affected by both charge and electrolyte screening effects [39]. The electrolyte concentration of NaCl in the pH dependent experiments was kept constant. However, the electrolyte concentration is determined not just by NaCl concentration but also by free H+ click here and Cl− ions in solution [40]. A lowering of the pH will therefore increase the screening of the protein in the same manner achieved by adding salt. Based

upon the arguments presented above and on the results discussed in Section 3.1, decreasing the colloidal stability decreases the radius of spherulites. This is in agreement with what is observed in the region pH 1–1.75 (Fig. 5). At pH 1.75–2 BCKDHA an abrupt change is observed in the size of the final spherulites which is unlikely to be purely due to factors affecting colloidal stability. Haas et al. [41] examine the conformational flexibility of bovine insulin as a function of pH. In simulations of the conformational space sampled by the protein chain they found a significant difference in behaviour in the regions pH 1–2 and 2–5: the C terminal of the B chain on the insulin molecule can sample a much wider conformational space at higher pH resulting in

a significant difference in the entropic contribution to the free energy barrier. The B-chain’s C-Terminal is known to play an important role in insulin fibrillation. Brange et al. suggest that the B-chain’s C terminus must be displaced in order to expose key hydrophobic residues involved in fibril formation [42]. Moreover, insulin degradation at the Asn21 residue is a possibility under these highly acidic conditions providing an alternative possible explanation of the observed effects [43]. However it should also be noted that the crystal structure of insulin at pH 2 shows no evidence of degradation [44]. A higher conformational flexibility of this terminal would therefore lead to a higher probability of the molecule losing its native structure under conditions conducive to aggregation.

, 2005). Given this limitation, measurements of conjugated or total BPA may be useful surrogates of free BPA. Specifically, FG-4592 datasheet if there is small variation in the ratio of free to conjugated BPA within and between individuals (with respect to the variation in exposure levels), then conjugated or total BPA may be an accurate and precise surrogate of free BPA, and of BPA exposure in general. This example underscores the importance of understanding relationships between exposure and biomarkers, different types of biomarkers

(parent vs. metabolites in their respective matrices), and biomarkers and biological targets, while ensuring that the appropriate research question is addressed. It further highlights the possibility of trade-offs when selecting an individual biomarker of exposure (for BPA, biological relevance could be optimized at the expense of ability to detect the chemical). A Tier 1 biomarker of exposure in a specified matrix is an accurate and precise surrogate of target dose (for hypothesis-driven studies with a known target) or of external exposure (for studies without a known target). For a Tier 2 biomarker, evidence exists for a relationship between the biomarker in a specified matrix and external exposure, learn more internal dose, or target dose. A Tier 3 biomarker in a specified matrix is a poor surrogate (low accuracy and precision) for exposure/dose. It can be challenging in epidemiological

studies to perform meaningful comparisons of short-lived biomarker measurements and long-term health 6-phosphogluconolactonase outcomes. Particularly in cross-sectional studies, a key assumption is that current biomarker levels reflect past exposures during time windows that were relevant for disease onset. Biomarkers of effect offer a means to evaluate exposure–response relationships

in target populations, during critical time windows, prior to disease onset. Findings are interpreted based on the strength of association between biomarkers of exposure and effect, and between biomarkers of effect and the adverse health outcome. The progression from an exposure event to an adverse health effect can be defined using adverse outcome pathways (AOPs) (Ankley et al., 2010). The AOP for a particular health outcome begins with a molecular initiating event at a target within the body. Effects at the molecular target, initiated by exposure events, progress to effects at the cellular, tissue, and organ levels, and ultimately to the whole organism. “Key events” are intermediate steps along the AOP that can be experimentally monitored to evaluate progression along the AOP. Measurements of these key events in accessible biological media from living intact organisms are called bioindicators. Bioindicators are considered ideal biomarkers of effect because they reflect a biological function linked to a specific adverse outcome; they “provide a high degree of confidence in predicting the potential for adverse effects in an individual or population” (www.epa.gov/pesticides/science/biomarker.

exogenous control over spatial attention. Before we elaborate on our choice of control settings, we first develop our general theoretical and empirical approach. A benchmark Vorinostat price result in the task-switching literature is the so-called switch-cost asymmetry. When people switch between a dominant task, such as Stroop

word naming and a competing, non-dominant task, such as Stroop color naming, switch costs are larger when transitioning from the hard, non-dominant to the easy, dominant task than the other way round (e.g., Allport et al., 1984). This phenomenon is important here because carry-over models of task switching seem to be able to explain it in a straightforward manner: Non-dominant tasks require a particularly strong attentional setting to survive against the

competition from the dominant task and this strong setting is carried forward into the next trial where it needs to be overcome when switching back to the dominant task. In contrast, the dominant task requires only weak support from a task setting and therefore relatively speaking, less change in control settings is required when switching from the dominant to the non-dominant task. Critically, selleck kinase inhibitor for the carry-over account to work, trial-to-trial switching between the two competing tasks is a necessary condition for obtaining a switch cost asymmetry (Gilbert and Shallice, 2002, Yeung and Monsell, 2003a and Yeung and Monsell, 2003b). Even though this model adequately accounts for the not basic finding of the asymmetry in switch costs, there is also some initial evidence that directly contradicts the carry-over account. Obviously, the carry-over account can explain the task-selection cost asymmetry only for cases

in which the alternative task was performed in the immediately preceding trial––otherwise there would be no opportunity for carry-over. However, Bryck and Mayr (2008) have shown that a cost asymmetry can be obtained even in the absence of a task-switch transition (see also Allport & Wylie, 2000). This finding, which will be elaborated below, is important because it indicates that opportunity for trial-to-trial carry-over is not a necessary condition for the cost asymmetry to arise. A key tenet of our account is that interference comes not from the most recent past (i.e., the previous trial), but from any kind of previous experiences with the competing tasks that are stored in long-term memory. One long-term memory model that is particularly well-equipped to handle the influence of past task experiences is memory instance theory (Hintzman, 1986 and Logan, 1988). To fully explain task-selection costs, this theory needs to be augmented through additional assumptions about factors that affect encoding and retrieval of memory instances.