C57BL/6 mice are widely used for experimental studies since the majority of genetically modified mice are bred on this background [10]. In an initial pilot study the response to loading in male mice appeared inconsistent and markedly lower than that in females. Since this was unexpected [7] and [11] we investigated the behaviour of these mice. Differences in behaviour between group-housed males and females led us to perform the study we report here in which the response to unilateral tibial loading in animals housed individually was compared to that in animals housed

in groups. Sixteen-week-old male and female C57BL/6 mice were obtained from Charles River Inc. (Margate, UK) and, although prior to delivery they were housed NVP-BGJ398 mw in groups, fighting was reported to occur infrequently between males and not at all in females (personal communication). Within 24 h of arrival, five male and five female mice were sacrificed for ex vivo strain measurements (see later). Of the remaining animals, six males and six females were housed in individual cages and six of each sex were kept as a single group for five days before the study commenced. All mice

were allowed free access to water and a maintenance diet containing 0.75% calcium (EURodent Diet 22%; PMI Nutrition International, LLC, Brentwood, MO, USA) in a 12-hour light/dark cycle, with room temperature at 21 ± 2 °C. All cages contained wood shavings, bedding and a cardboard tube for environmental enrichment. For one hour directly preceding each episode of in vivo loading, grouped mice were observed and any aggressive behaviour or fighting was recorded. The hour during which Epacadostat molecular weight HSP90 mice were observed was always at the same time of day in the morning, one hour after the start of the light period, by the same observer (LBM). All procedures complied with the UK Animals (Scientific Procedures) Act 1986 and were reviewed and approved by the University of Bristol ethics committee (Bristol, UK). To apply similar magnitudes of peak strain in male and female mice, we first established

the strain:load relationship ex vivo in the sub-sample of five male and five female mice. In each mouse, a single element strain gage (EA-06-015DJ-120, Vishay Measurement Group, NC) was bonded longitudinally to the medial aspect of the tibia at 37% of its length from the proximal end. This is the site where we have previously observed the greatest osteogenic response to axial loading [12]. Strains were measured across a range of peak loads between 5 and 17 N, applied using the same electromagnetic loading machine used for in vivo loading (ElectroForce 3100; Bose Co., Eden Prairie, MN, USA). Linear regression analysis allowed calculation of the loads required to apply 2200 με at the start of the study. Right tibiae were subjected to external mechanical loading under isoflurane-induced anesthesia on alternate days for two weeks.

The recorded image data of our study consist of a complete Raman spectrum per pixel. From these data chemical maps of the contained compounds can be extracted. Subsequently, color coded overlay images can be prepared and utilized to determine the spatial distribution of hydrohalite and cellular matter. In some cases the overlay images are ambiguous with respect to the hydrohalite localization – mostly due to the limited axial resolution – and specific characteristics in colocalization plots are found to be helpful in the further interpretation of the data. Spatial correlation between hydrohalite and cellular matter

will show up in colocalization plots and can be used to determine whether the hydrohalite is located within or outside the cell. It is indeed Nutlin-3 solubility dmso shown, that hydrohalite can form inside cells under certain conditions, though it seems less serious in established cryopreservation protocols in vital biobanking. However, it has to be considered in the study of cryoinjury mechanisms. The

experimental setup consists of three elements; A confocal Raman microscope, a temperature controlled chamber Lonafarnib in vitro and a scanning stage. We measured the point spread function giving a radial and axial FWHM of 0.8 μm and 2.5 μm for the optical setup. Further details on the experimental setup can be found in [10]. For the example Raman spectra of Me2SO and cellular matter shown in Fig. 1a two samples at room temperature containing either pure Me2SO (WAK-Chemie GmbH, Germany) or mouse fibroblasts in PBS (PAN Biotech GmbH, Germany) were used. Two additional samples were used for the Raman spectra of ice and hydrohalite, which was recorded at a temperature of approximately −20 °C using solutions of 25 wt.% NaCl saline solution or demineralised water. The integration time for these Raman spectra is 2 s. The Raman images are recorded using adherent mouse fibroblasts in

PBS (PAN Biotech GmbH, Germany) and are cooled to −50 °C at a cooling rate of −1 °C/min. The integration time for each pixel is 100 ms and the others images have a scan area of 50 μm × 50 μm. The investigated samples were equilibrated a few minutes in either PBS without Me2SO or with 0.5 wt.% Me2SO at room temperature before the cooling protocol were applied. The sample volume was approximately 10 μL, which corresponds to a sample height of ≈40 μm. The investigated cell line is the L929 mouse fibroblast from ATCC (United States). The cells were incubated at 37 °C and a 5% CO2 atmosphere in Gibco© Dulbecco’s modified Eagle medium (Life Technologies, United States) with 10% fetal calf serum on glass cover slips (VWR, United States). The cells were handled using standard procedures. We use confocal Raman microscopy to investigate the solid states that form in cryopreservation samples upon cooling. The Raman spectra of the compounds encountered in this study are shown in Fig. 1a.

A existência de diferenças entre os grupos relativamente ao uso de IBP, tendo estes sido mais utilizados no ano de maior incidência de DACd (2008; p = 0,02) também se encontra descrita na literatura 21. Embora existam dados contraditórios em relação ao papel dos IBP na aquisição da DACd em meio hospitalar, experiências feitas em ratos de laboratório e estudos de base populacional relativos à aquisição da doença na comunidade têm fornecido dados consistentes que fundamentam os IBP

como fator de risco independente. Parece que o seu mecanismo de ação, proporcionando o aumento do pH gástrico, favorece a sobrevivência da bactéria e deste modo facilita a aquisição da infeção – alterações na resposta see more leucocitária e o aumento da produção de toxinas são possíveis mecanismos adicionais 22 and 23. Para além disto, os IBP são dos fármacos mais prescritos atualmente, o que também poderá ajudar a compreender a diferença encontrada entre os 2 grupos. Relativamente ao método de diagnóstico da DACd, encontraram-se diferenças com significado estatístico entre os 2 grupos, sendo a pesquisa de toxinas mais utilizada em 2008 (p <0,01). Até ao ano de 2006, não foi possível apurar qual o teste de pesquisa de toxinas utilizado no nosso hospital, sabendo-se só que detetava unicamente a toxina A, levando provavelmente a um maior

Ibrutinib price recurso à endoscopia digestiva baixa como teste de diagnóstico. Os testes imunoenzimáticos mais recentes já apresentam sensibilidade e especificidade elevadas quando comparados com o teste-padrão, que se baseia na citotoxicidade celular, mas estes resultados não se mantêm quando a prevalência das toxinas nas fezes é inferior a 10%, baixando o seu valor preditivo positivo 24. No ano de 2008, registou-se também um maior número de casos complicados, sendo a diferença significativa relativamente aos outros anos (p = 0,01). A tendência para um incremento das complicações e da mortalidade

já foi observada e relatada noutros estudos, maioritariamente associada a uma estirpe Branched chain aminotransferase mais virulenta de C. difficile, mas também à existência de mais comorbilidades e de idade superior nas populações afetadas 11. Relativamente à idade, não encontramos diferenças entre os grupos, mas não averiguámos as comorbilidades nem o tipo de estirpe presente, pelo que serão necessários mais estudos para corretamente abordar esta questão. Em 2008, no nosso estudo verificámos um aumento na incidência de casos de DACd relativamente aos outros anos (2000-2007). Documentou-se igualmente um maior uso de carbapenemes e de IBP nesta população de doentes em 2008. O principal método de diagnóstico utilizado foi a pesquisa de toxinas, por meio de teste imunoenzimático, em oposição à endoscopia digestiva baixa, mais usada nos outros anos.

The blood cells are deformed in capillaries where physical/chemical reactions take place. However blood cells are also occasionally transported into these recirculation zones in larger blood vessels, at bends and bifurcations. mTOR tumor The cells remain in the recirculation zones over several pulse cycles and are subjected to both high and low shear stresses. Many papers use the term ‘turbulent flow’, however a true turbulent flow is found only in the ascending aorta and this is not fully developed because of the entrance length. Everywhere else you will have a nominal, laminar or transitional flow. The definition for laminar and turbulent flow is: Laminar flow The

fluid elements move parallel to each other in distinct paths. In all layers the velocity (fluid elements) moves tangentially to the main flow. Nominal laminar Small velocity

fluctuations are added to laminar flow. This flow is characterized I BET 762 by small velocity disturbances. Transitional flow is laminar flow with spatial and temporal velocity disturbances (fluctuations), which decreases relatively quickly distal to the local flow disturbance. It is a flow between laminar and turbulent, where flow disturbances disappear over time. Turbulent flow Three-dimensional, spatial and temporal velocity fluctuations are superimposed on the main flow direction. The flow becomes irregular and chaotic. Full-size table Table options View in workspace Download as CSV A fully developed laminar profile creates a parabolic velocity profile (1) and a fully turbulent flow creates a very flat velocity profile (2). The flow behavior can

be calculated with a dimensionless parameter called Reynolds number (Re-number). The Re-number can be calculated with the average velocity over the cross section of the vessel, the diameter and the kinematics viscosity. Re = (u·d/ν) = ( Fig. 1) For pulsatile flow the Reynolds number should be calculated with a flow rate over one pulse cycle u=V/A→Re=4 V⋅dΠd2υ=4VΠdπNormally, you will never find Reynolds Interleukin-3 receptor numbers higher than 2300 in blood vessels using the above definition. The entrance length is too short and the pulse wave cannot develop into a turbulent flow. The non-Newtonian flow behavior of blood can be neglected in straight pipes because the profile is only 3–4% different compared to a fully developed paraboloid in a straight pipe (Fig. 1 right, white arrow). The influence of the bifurcation angle and the stenosis degree were studied. We used 1:1 true-to scale, elastic silicon rubber models with a compliance similar to that of the arterial wall. This special technique was described in Biorheology 23, 1986. The surface in the model reproduces the biological vessel surface. The carotid artery models were installed in a physiologically accurate circulatory system. The fluid was a polyacrylamid mixture and a water solution which shows a flow behavior similar to that of human blood.

Das Abtasten von Strumen in Regionen mit mildem Iodmangel ist von geringer Sensitivität und Spezifität; in diesen Gebieten sollte die Bestimmung des Schilddrüsenvolumens zur Einstufung von Strumen vorzugsweise durch Sonographie erfolgen [28]. Bei Untersuchungen vor Ort können tragbare Ultraschallgeräte eingesetzt werden, und Strumen können entsprechend den internationalen Referenzkriterien für ausreichend

mit Iod versorgte Kinder nach Alter, Geschlecht und Körperoberfläche Atezolizumab in vitro klassifiziert werden [29]. Die Struma-Gesamthäufigkeit wird unter Anwendung der folgenden Kriterien zur Definition des Schweregrades verwendet: < 5%: ausreichende Versorgung; 5,0 bis 19,9%: milder Iodmangel; 20,0 bis 29,9%: moderater Iodmangel und > 30%: schwerer Iodmangel [1]. Obwohl das Schilddrüsenvolumen als Antwort auf eine höhere Iodaufnahme erwartungsgemäß abnimmt, stellen sich in Gebieten mit endemischer Struma möglicherweise auch Monate oder Jahre nach Beseitigung des Iodmangels keine normalen Schilddrüsenvolumina ein [30]. Während dieser Übergangsphase ist die Strumahäufigkeit schwierig zu interpretieren, da sie gleichzeitig die Vorgeschichte der Iodversorgung Crizotinib einer Population als auch deren aktuellen

Status widerspiegelt. Ein nachhaltiges Salz-Iodierungsprogramm senkt die mittels Sonographie bestimmte Strumahäufigkeit bei Schulkindern auf < 5% [31], und dies zeigt an, dass der Iodmangel als bedeutendes Problem der öffentlichen Gesundheit beseitigt ist [1]. Da mehr als 90% des aufgenommenen Iods mit Dehydratase dem Urin ausgeschieden werden, ist die UI ein ausgezeichneter Indikator der aktuellen

Iodaufnahme. Die meisten Methoden zur Messung der UI basieren auf der Sandell-Kolthoff-Reaktion, bei der Iodid in Gegenwart von arseniger Säure die Reduktion des gelben Ammoniumcer(IV)-sulfats zur farblosen Cer(III)-Form katalysiert. Die Iodausscheidung im Urin kann als Konzentrationswert (μg/L), im Verhältnis zur Kreatininausscheidung (μg Iod/g Kreatinin) oder als 24-Stunden-Ausscheidung (μg/Tag) angegeben werden. Da in Feldstudien aus praktischen Gründen keine 24-Stunden-Urinproben gesammelt werden können, kann die UI in Spontanurinproben einer repräsentativen Stichprobe der jeweiligen Zielbevölkerung bestimmt und als Median in μg/L ausgedrückt werden [1]. Variationen zwischen Einzelpersonen hinsichtlich der Flüssigkeitszufuhr gleichen sich bei einer großen Anzahl von Proben im Allgemeinen aus, so dass die mediane UI in Spontanurinproben gut mit der in 24-Stunden-Proben korreliert.

The RH inside the cell was always lower than the outside, and water vapor transport was determined from the weight gain of

the permeation cell. After steady state conditions were reached (about 2 h), ten weight measurements were made over 48 h. WVP was calculated according Equation (1): equation(1) WVP=(w/θ)×[(24×t)/(A×Δp)]WVP=(w/θ)×[(24×t)/(A×Δp)] wherein: WVP is the water vapor permeability [g mm m−2 d−1 kPa−1]; NLG919 w is the weight gain (from the straight line) [g]; θ is the time during which w occurred [h]; t is the average film thickness [mm]; A is the test area (cell top area) [m2] and Δp is the vapor pressure difference [kPa]. All specimens were evaluated in triplicate. Oxygen transmission rate (OTR) [cm3 m−2 d−1] of the films was measured at 23 °C and 75% RH on a 50 cm2 circular films using an oxygen permeation system (OXTRAN 2/21, MOCON, USA), in accordance

with ASTM F1927-07 (2007). A starch based film was sealed between two chambers (each one with two channels), the lower one supplied with O2 at a controlled flow rate (20 mL min−1) to keep the pressure constant in that compartment, and the other one was purged by a stream of nitrogen carrier gas (0.98 part of nitrogen and 0.02 part of hydrogen), at controlled flow rate (10 mL min−1). A colorimetric sensor determined the amount of oxygen transmitted through the film into the carrier gas. The oxygen find more Methane monooxygenase transmission rate was determined for all specimens in duplicate. The permeance (PO2) of the films was calculated according to Equation (2): equation(2) PO2=OTR/pPO2=OTR/pwherein: PO2 is the permeance of the films [cm3 m−2 d−1 Pa−1];

OTR is the oxygen transmission rate [cm3 m−2 d−1]; and p is the partial pressure of oxygen, which is the mol fraction of oxygen multiplied by the total pressure (nominally, one atmosphere), in the test gas side of the diffusion cell. The partial pressure of O2 on the carrier gas side is considered zero. The oxygen permeability coefficient (P′O2) was calculated as follows: equation(3) P′O2=PO2×tP′O2=PO2×twherein: P′O2 is the oxygen permeability coefficient [cm3 m−1 d−1 Pa−1]; and t is the average thickness of the specimen [mm]. Glass transition temperature (Tg) of BF was determined by differential scanning calorimetry, using a DSC TA 2010 controlled by a TA 4000 module (TA Instruments, New Castle, USA), with a quench cooling accessory, operated with nitrogen at 150 mL min−1. Temperature and melting enthalpy calibrations were performed with indium and bidistilled water and Milli-Q. Samples of about (2–5) mg were weighed in a precision balance (Scientech, SA210, USA), conditioned in hermetic aluminum pans (20 μL), and submitted to a temperature program, under inert atmosphere (100 mL min−1 of N2). In the first scan, after cooling the sample at −10 °C min−1 up to −60 °C, it was submitted to heating at 10 °C min−1 until 100 °C.

It is made up of tight junctions between endothelial cells on cranial capillaries, a thick basement membrane and astrocytic end-feet. The BBB serves to restrict bacteria and other large hydrophilic molecules from entering the brain

click here parenchyma, while allowing small hydrophobic molecules and nutrients to enter. Pharmacologic treatment of neurologic diseases has relied on brain penetration of small lipophilic molecules. However, where high selectivity and potency is desirable, an alternative therapeutic approach could be the use of monoclonal antibodies (mAbs). Immunoglobulin-Gs (IgGs), along with other plasma proteins, are large hydrophilic molecules that are unable to pass through the BBB in sufficient quantity to be efficacious when systemically administered (Poduslo et al., 1994). Researchers are currently

experimenting with receptor-based brain endothelial transcytosis, such as using the transferrin receptor (Bickel et al., 1994, Pardridge et al., 1991 and Yu et al., 2011) or insulin receptor (Boado et al., 2007 and Pardridge et al., 1995) for IgGs to enter the brain parenchyma. However, once mAbs enter the brain, the extent to which they are cleared by receptor-mediated reverse transcytosis is not well-known. Evidence of the involvement of an Fc-receptor in the clearance of IgG from the central nervous system (CNS) has been shown by a DAPT shorter half-life of IgG, compared to IgM (antibody that lacks Fc region), in both rat and monkey cerebrospinal fluid (Bergman et al., 1998). Moreover, efflux of IgG though the BBB is competitively inhibited by the addition of Fc fragments (Boado et al., 2007 and Zhang and Pardridge, 2001). Indeed, the Fc-receptor mediated Aβ-IgG efflux mechanism has been shown to facilitate the clearance of IgG complexes from brains (Deane Cisplatin in vivo et al., 2005). There are data to both support and refute the role of the neonatal Fc-receptor (FcRn) in IgG efflux from the brain. Using non-compartment mathematical modeling

in mice which lack FcRn functionally, there was no apparent difference in efflux compared to wild-type mice based on labeled IgG and residual blood volume (Abuqayyas and Balthasar, 2013 and Garg and Balthasar, 2009). FcRn is visualized by confocal microscopy in brain microvasculature endothelial cells (Schlachetzki et al., 2002), but whether the receptor is involved in efflux in addition to its role in recycling IgG is unknown. In vascular endothelial cells, IgG is taken up from the circulation by non-specific fluid-phase pinocytosis where it binds to FcRn in the acidic endosome. It is recycled to the capillary lumen where it has a long half-life (Roopenian and Akilesh, 2007). It is therefore postulated that expression of FcRn located in brain endothelial cells (Schlachetzki et al., 2002) may be involved in the efflux of IgGs from the brain.

To demonstrate the quality of their dataset, Cheung et al. subdivided their dataset along the mutational status of KRAS, BRAF and PIK3CA, genes frequently mutated in human cancers. Cells harboring such activated oncogenes frequently depend on their continued activity to maintain a malignant phenotype, a phenomenon called ‘oncogene addiction’ [ 15]. Reassuringly, comparing the phenotypes of mutant and wildtype cell lines consistently pinpointed the known oncogene – KRAS, BRAF or PIK3CA, respectively – as specifically required LY2109761 price for cell growth only in the presence of the activating mutation. Next, the researchers split their dataset according to the cell lines’ tissue

of origin instead. Searching for genes required specifically for proliferation and/or survival of ovarian cancer cells revealed a set of ∼600 genes, a subset of which had previously been reported to be amplified or overexpressed in ovarian tumors (9.5%, 55/582). The differential phenotype of one of them, the transcription factor PAX8, was tested in eight ovarian cancer cell lines: six of them relied on PAX8 expression for continued growth. In an independent study, Brough et al. employed a similar strategy to identify differential growth and viability phenotypes in a panel of 34 breast p38 MAPK activation cancer cell lines [ 16•]. They recorded the effects

of targeting ∼700 kinases with pooled siRNAs and then split the dataset according to the cell lines’ genetic markers, including common amplification events (e.g. of the ERBB2 locus), known

mutations (e.g. in Amisulpride PIK3CA) or clinical subtypes (e.g. ER+/ER−). The researchers identified multiple RNAi phenotypes specifically associated with cancer-associated genetic aberrations: For example, cells lacking functional copies of the tumor suppressor gene PTEN were particularly dependent on genes controlling the mitotic spindle assembly checkpoint and showed synthetic lethality with siRNAs as well as small molecule inhibitors targeting the checkpoint kinase TTK [ 16• and 17]. These examples highlight how the phenotypic differences within a panel of cell lines can reveal shared dependencies of tumor subtypes, potentially providing a highly selective set of candidate drug targets. Recently, this approach has also been applied to address a long-standing challenge in cancer research: how to kill tumors carrying mutations in the gene most frequently affected in human cancers – RAS? More than 30% of tumors carry mutations in members of the RAS small GTPase protein family, making NRAS, KRAS and HRAS the most commonly affected genes in human cancers [18]. Many cancer cell lines have also remained addicted to constant activity of the Ras-signaling pathway for maintaining a malignant phenotype, rendering RAS (and other pathway members including, for example, its downstream effector BRAF) highly attractive drug targets [19••].

Each compound screening assay freeze-dried sample was mixed with anhydrous sodium sulfate, ground with mortar, and pestled to obtain a dry powder. The powdered mass was then extracted with dichloromethane using an ASE 200 extractor (Dionex, Salt Lake City, UT, USA). The extracted volume was reduced to ∼1.5 ml using a rotary evaporator and then fractionated through an alumina oxide column to remove polar interferences using 35 ml of petroleum ether. The extract was concentrated to ∼5 ml by rotary evaporation and transferred to a pre-combusted, glass test tube. The extract volume was further reduced to ∼1 ml using a purified nitrogen stream and sealed in an amber vial

for GC-MS analysis. The sample analysis was performed by a Varian 3800GC/Saturn 4000 ion trap mass spectrometer (Varian, Walnut Creek, CA, USA) operated in the ion-monitoring mode. Prior to the analysis, a mixture of perdeuterated PAHs, including phenanthrene-d10, benzo(a)anthracene-d10, benzo(a)pyrene-d12,

and benzo(g,h,i)perylene-d12, was added immediately to each extract as an internal standard. Each PAH was identified by its retention time relative to the internal standards and quantified by comparing the integrated NLG919 mouse area of the molecular ion chromatogram to that of the internal standard ( Ko and Baker, 1995 and Ko and Baker, 2004). The detailed description about the PAH’s analysis can be found in Hung et al (2010). The concentrations of PAHs in zooplankton at 27 stations (excluding station 30 due to sample spilling) are expressed in two different units: ng g−1 (e.g., PAHs normalized by dry weight of zooplankton) and ng m−3 (e.g., PAH concentrations (ng g−1) normalized by zooplankton biomass in seawater (g m−3)). There

are at least four main water masses (Fig. 1, CDW: Changjiang Diluted Water, TCWW: Taiwan Current Warm Water, KW: the Kuroshio Water, YS: Yellow Sea Water) in the ECS in April based on temperature and salinity distributions (Fig. 1 and Fig. 2 and Table 1). CDW is a mixture of Changjiang River runoff and shelf water with low salinity and high nutrient concentrations (Gong et al., 2003 and Hung et al., 2013). YSW is mainly carried into the northern part of the ECS through the Chinese Coastal Current from the Yellow Sea (Ichikawa and Beardsley, 2002), showing moderate salinity, Phosphoglycerate kinase low temperature and low nutrient concentrations (Gong et al., 2003 and Chou et al., 2009). TCWW enters the ECS from the Taiwan Strait with high temperature and high salinity (Gong et al, 2003), but its salinity is lower than that of the KW. The KW flows northeast along the shelf with high temperature, high salinity and low nutrient concentrations (Gong et al., 2003 and Hung et al., 2009b). As a whole, the hydrographic setting in this survey in spring was similar to that reported for previous investigations (Gong et al., 2003 and Chou et al., 2009). Fig. 2 shows contour maps of surface salinity, NO3−, Chl-a and plankton biomass in the ECS.

Analyses of neural activities at the end of the secondary task showed another important facet of interference effects ABT-199 supplier in the LPFC. Watanabe and Funahashi [33••] found a significant ‘reawakening’ of neural encoding for

the visual cue location in the memory task after the end of the attention task (Figure 3e), which indicates that even under the presence of the interference effect caused by the attention task, some neural mechanisms in the LPFC could operate to compensate for the interference effect produced by the attention task. Similar results have been reported by Miyazaki et al. [32], who compared the activities of LPFC neurons and dorsal premotor neurons while monkeys performed a dual task, which consisted of memory-guided bimanual actions (primary task) and visually-guided bimanual actions (secondary task). The observed post-interference reactivation of the primary-task information showed that the LPFC played an important

role in exerting compensatory control over the interference by the secondary task. Flexible prioritization among multiple streams of concurrent task processing is critical for the coordination of dual-task performance. The observed reactivation may correspond to the neural implementation of adaptive task coordination TGFbeta inhibitor in the LPFC 22 and 24. Behavioral analyses and physiological investigations of dual-task interference using monkeys are beginning to provide evidence regarding the neural mechanisms for interference control. The similarity of the behavioral patterns caused by dual-task interference in humans and monkeys and the capability Benzatropine to elucidate the fine details of neural computations by neurophysiological methods support the view that the primate model

is an appropriate method for understanding the details of the neural mechanisms of the interference control and the flexible allocation of cognitive recourse. Nothing declared. Papers of particular interest, published within the period of review, have been highlighted as: • of special interest This work was supported in part by Grant-in-Aids for Scientific Research (Nos. 21240024 and 25240021) from the Japanese Ministry of Education, Culture, Sports, Science and Technology (MEXT) to SF and by Research Fellowships for Young Scientists from the Japan Society for the Promotion of Science to KW. “
“Current Opinion in Behavioral Sciences 2015, 1:17–22 This review comes from a themed issue on Cognitive neuroscience Edited by Cindy Lustig and Howard Eichenbaum http://dx.doi.org/10.1016/j.cobeha.2014.07.006 2352-1546/© 2014 Elsevier Ltd. All right reserved. One of the most prominent aspects of cognitive control has been characterized as ‘inhibition’ or inhibitory processing.