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51.
A cognitive neurobiological account of deception: evidence from functional neuroimaging 总被引:5,自引:0,他引:5
Spence SA Hunter MD Farrow TF Green RD Leung DH Hughes CJ Ganesan V 《Philosophical transactions of the Royal Society of London. Series B, Biological sciences》2004,359(1451):1755-1762
An organism may use misinformation, knowingly (through deception) or unknowingly (as in the case of camouflage), to gain advantage in a competitive environment. From an evolutionary perspective, greater tactical deception occurs among primates closer to humans, with larger neocortices. In humans, the onset of deceptive behaviours in childhood exhibits a developmental trajectory, which may be regarded as 'normal' in the majority and deficient among a minority with certain neurodevelopmental disorders (e.g. autism). In the human adult, deception and lying exhibit features consistent with their use of 'higher' or 'executive' brain systems. Accurate detection of deception in humans may be of particular importance in forensic practice, while an understanding of its cognitive neurobiology may have implications for models of 'theory of mind' and social cognition, and societal notions of responsibility, guilt and mitigation. In recent years, functional neuroimaging techniques (especially functional magnetic resonance imaging) have been used to study deception. Though few in number, and using very different experimental protocols, studies published in the peer-reviewed literature exhibit certain consistencies. Attempted deception is associated with activation of executive brain regions (particularly prefrontal and anterior cingulate cortices), while truthful responding has not been shown to be associated with any areas of increased activation (relative to deception). Hence, truthful responding may comprise a relative 'baseline' in human cognition and communication. The subject who lies may necessarily engage 'higher' brain centres, consistent with a purpose or intention (to deceive). While the principle of executive control during deception remains plausible, its precise anatomy awaits elucidation. 相似文献
52.
53.
Proliferating cell nuclear antigen (PCNA) as a proliferative marker during embryonic and adult zebrafish hematopoiesis 总被引:4,自引:1,他引:3
Leung AY Leung JC Chan LY Ma ES Kwan TT Lai KN Meng A Liang R 《Histochemistry and cell biology》2005,124(2):105-111
We investigated the expression of proliferative cell nuclear antigen (PCNA) in zebrafish to delineate the proliferative hematopoietic
component during adult and embryonic hematopoiesis. Immunostaining for PCNA and enhanced green fluorescence protein (eGFP)
was performed in wild-type and fli1-eGFP (endothelial marker) and gata1-eGFP (erythroid cell marker) transgenic fish. Expression
of PCNA mRNA was examined in wild-type and chordin morphant embryos. In adult zebrafish kidney, the renal tubules are surrounded
by endothelial cells and it is separated into hematopoietic and excretory compartments. PCNA was expressed in hematopoietic
progenitor cells but not in mature neutrophils, eosinophils or erythroid cells. Some PCNA+ cells are scattered in the hematopoietic
compartment of the kidney while others are closely associated with renal tubular cells. PCNA was also expressed in spermatogonial
stem cells and intestine crypts, consistent with its role in cell proliferation and DNA synthesis. In embryos, PCNA is expressed
in the brain, spinal cord and intermediate cell mass (ICM) at 24 h-post fertilization. In chordin morphants, PCNA is significantly
upregulated in the expanded ICM. Therefore, PCNA can be used to mark cell proliferation in zebrafish hematopoietic tissues
and to identify a population of progenitor cells whose significance would have to be further investigated. 相似文献
54.
Aminoacyl-tRNA synthetases establish the rules of the genetic code by aminoacylation reactions. Occasional activation of the wrong amino acid can lead to errors of protein synthesis. For isoleucyl-tRNA synthetase, these errors are reduced by tRNA-dependent hydrolytic editing reactions that occur at a site 25 A from the active site. These reactions require that the misactivated amino acid be translocated from the active site to the center for editing. One mechanism describes translocation as requiring the mischarging of tRNA followed by a conformational change in the tRNA that moves the amino acid from one site to the other. Here a specific DNA aptamer is investigated. The aptamer can stimulate amino acid-specific editing but cannot be aminoacylated. Although the aptamer could in principle stimulate hydrolysis of a misactivated amino acid by an idiosyncratic mechanism, the aptamer is shown here to induce translocation and hydrolysis of misactivated aminoacyl adenylate at the same site as that seen with the tRNA cofactor. Thus, translocation to the site for editing does not require joining of the amino acid to the nucleic acid. Further experiments demonstrated that aptamer-induced editing is sensitive to aptamer sequence and that the aptamer is directed to a site other than the active site or tRNA binding site of the enzyme. 相似文献
55.
James R. Rudd Lisa M. Barnett Michael L. Butson Damian Farrow Jason Berry Remco C. J. Polman 《PloS one》2015,10(10)
Introduction
In motor development literature fundamental movement skills are divided into three constructs: locomotive, object control and stability skills. Most fundamental movement skills research has focused on children’s competency in locomotor and object control skills. The first aim of this study was to validate a test battery to assess the construct of stability skills, in children aged 6 to 10 (M age = 8.2, SD = 1.2). Secondly we assessed how the stability skills construct fitted into a model of fundamental movement skill.Method
The Delphi method was used to select the stability skill battery. Confirmatory factor analysis (CFA) was used to assess if the skills loaded onto the same construct and a new model of FMS was developed using structural equation modelling.Results
Three postural control tasks were selected (the log roll, rock and back support) because they had good face and content validity. These skills also demonstrated good predictive validity with gymnasts scoring significantly better than children without gymnastic training and children from a high SES school performing better than those from a mid and low SES schools and the mid SES children scored better than the low SES children (all p < .05). Inter rater reliability tests were excellent for all three skills (ICC = 0.81, 0.87, 0.87) as was test re-test reliability (ICC 0.87–0.95). CFA provided good construct validity, and structural equation modelling revealed stability skills to be an independent factor in an overall FMS model which included locomotor (r = .88), object control (r = .76) and stability skills (r = .81).Discussion
This study provides a rationale for the inclusion of stability skills in FMS assessment. The stability skills could be used alongside other FMS assessment tools to provide a holistic assessment of children’s fundamental movement skills. 相似文献56.
57.
Cugini C Calfee MW Farrow JM Morales DK Pesci EC Hogan DA 《Molecular microbiology》2007,65(4):896-906
58.
Emmanuel Risse Andrew J. Nicoll William A. Taylor Daniel Wright Mayank Badoni Xiaofan Yang Mark A. Farrow John Collinge 《The Journal of biological chemistry》2015,290(27):17020-17028
The prion protein (PrP) has been implicated both in prion diseases such as Creutzfeldt-Jakob disease, where its monomeric cellular isoform (PrPC) is recruited into pathogenic self-propagating polymers of misfolded protein, and in Alzheimer disease, where PrPC may act as a receptor for synaptotoxic oligomeric forms of amyloid-β (Aβ). There has been considerable interest in identification of compounds that bind to PrPC, stabilizing its native fold and thereby acting as pharmacological chaperones to block prion propagation and pathogenesis. However, compounds binding PrPC could also inhibit the binding of toxic Aβ species and may have a role in treating Alzheimer disease, a highly prevalent dementia for which there are currently no disease-modifying treatments. However, the absence of a unitary, readily measurable, physiological function of PrP makes screening for ligands challenging, and the highly heterogeneous nature of Aβ oligomer preparations makes conventional competition binding assays difficult to interpret. We have therefore developed a high-throughput screen that utilizes site-specifically fluorescently labeled protein to identify compounds that bind to PrP and inhibit both Aβ binding and prion propagation. Following a screen of 1,200 approved drugs, we identified Chicago Sky Blue 6B as the first small molecule PrP ligand capable of inhibiting Aβ binding, demonstrating the feasibility of development of drugs to block this interaction. The interaction of Chicago Sky Blue 6B was characterized by isothermal titration calorimetry, and its ability to inhibit Aβ binding and reduce prion levels was established in cell-based assays. 相似文献
59.
Sheung-Tak Cheng Rosanna WL Lau Emily PM Mak Natalie SS Ng Linda CW Lam Helene H Fung Julian CL Lai Timothy Kwok Diana TF Lee 《Trials》2012,13(1):1-10
Background
Patients with ST-elevation myocardial infarction (STEMI) not treated with primary or rescue percutaneous coronary intervention (PCI) are at risk for recurrent ischemia, especially when viability in the infarct-area is present. Therefore, an invasive strategy with PCI of the infarct-related coronary artery in patients with viability would reduce the occurrence of a composite end point of death, reinfarction, or unstable angina (UA).Methods
Patients admitted with an (sub)acute myocardial infarction, who were not treated by primary or rescue PCI, and who were stable during the first 48 hours after the acute event, were screened for the study. Eventually, we randomly assigned 216 patients with viability (demonstrated with low-dose dobutamine echocardiography) to an invasive or a conservative strategy. In the invasive strategy stenting of the infarct-related coronary artery was intended with abciximab as adjunct treatment. Seventy-five (75) patients without viability served as registry group. The primary endpoint was the composite of death from any cause, recurrent myocardial infarction (MI) and unstable angina at one year. As secondary endpoint the need for (repeat) revascularization procedures and anginal status were recorded.Results
The primary combined endpoint of death, recurrent MI and unstable angina was 7.5% (8/106) in the invasive group and 17.3% (19/110) in the conservative group (Hazard ratio 0.42; 95% confidence interval [CI] 0.18-0.96; p = 0.032). During follow up revascularization-procedures were performed in 6.6% (7/106) in the invasive group and 31.8% (35/110) in the conservative group (Hazard ratio 0.18; 95% CI 0.13-0.43; p < 0.0001). A low rate of recurrent ischemia was found in the non-viable group (5.4%) in comparison to the viable-conservative group (14.5%). (Hazard-ratio 0.35; 95% CI 0.17-1.00; p = 0.051).Conclusion
We demonstrated that after acute MI (treated with thrombolysis or without reperfusion therapy) patients with viability in the infarct-area benefit from a strategy of early in-hospital stenting of the infarct-related coronary artery. This treatment results in a long-term uneventful clinical course. The study confirmed the low risk of recurrent ischemia in patients without viability.Trial registration
ClinicalTrials.gov: NCT00149591. 相似文献60.
Oglesby AG Farrow JM Lee JH Tomaras AP Greenberg EP Pesci EC Vasil ML 《The Journal of biological chemistry》2008,283(23):15558-15567
In iron-replete environments, the Pseudomonas aeruginosa Fur (ferric uptake regulator) protein represses expression of two small regulatory RNAs encoded by prrF1 and prrF2. Here we describe the effects of iron and PrrF regulation on P. aeruginosa physiology. We show that PrrF represses genes encoding enzymes for the degradation of anthranilate (i.e. antABC), a precursor of the Pseudomonas quinolone signal (PQS). Under iron-limiting conditions, PQS production was greatly decreased in a DeltaprrF1,2 mutant as compared with wild type. The addition of anthranilate to the growth medium restored PQS production to the DeltaprrF1,2 mutant, indicating that its defect in PQS production is a consequence of anthranilate degradation. PA2511 was shown to encode an anthranilate-dependent activator of the ant genes and was subsequently renamed antR. AntR was not required for regulation of antA by PrrF but was required for optimal iron activation of antA. Furthermore, iron was capable of activating both antA and antR in a DeltaprrF1,2 mutant, indicating the presence of two distinct yet overlapping pathways for iron activation of antA (AntR-dependent and PrrF-dependent). Additionally, several quorum-sensing regulators, including PqsR, influenced antA expression, demonstrating that regulation of anthranilate metabolism is intimately woven into the quorum-sensing network of P. aeruginosa. Overall, our data illustrate the extensive control that both iron regulation and quorum sensing exercise in basic cellular physiology, underlining how intermediary metabolism can affect the regulation of virulence factors in P. aeruginosa. 相似文献