Our data add to previous localization studies by describing an unexpected variation between LA and basal nucleus of the amygdala (BA) in the neurochemical phenotype of NK1-expressing neurons and reveal the relative source of glutamatergic inputs that may activate these neurons, which in turn regulate fear and anxiety responses. C646 concentration (C) 2011 IBRO. Published by Elsevier Ltd. All rights reserved.”
“African swine fever virus (ASFV), the causative agent of one of the most devastating swine

diseases, has been considered exclusively cytoplasmic, even though some authors have shown evidence of an early stage of nuclear replication. In the present study, an increment of lamin A/C phosphorylation was observed in ASFV-infected cells as early as 4 h postinfection, followed by the disassembling of the lamina network close to the sites where the viral genome starts its replication. At later time points, this and other nuclear envelope markers were found in the cytoplasm of the infected cells. The effect of the infection on the cell nucleus was much more severe than previously expected, since a redistribution of other nuclear proteins, such as RNA polymerase II, the splicing speckle SC-35 marker, and the B-23 nucleolar marker, was observed from 4 h postinfection. All this evidence, together with the redistribution,

dephosphorylation, and subsequent degradation of RNA polymerase II after ASFV infection, suggests the existence of sophisticated mechanisms to regulate the nuclear machinery www.selleckchem.com/products/Thiazovivin.html during viral infection.”
“The last years have seen the emergence of many large-scale proteomics initiatives that have identified thousands of new protein interactions and macromolecular assemblies. However, unfortunately, only a few among the discovered complexes meet the high-quality standards required to be promptly used in structural studies. This has thus created an increasing gap between the number of known protein interactions Adenosine triphosphate and complexes and those for which a high-resolution 3-D structure is available. Here, we present and validate a computational strategy to distinguish those

complexes found in high-throughput affinity purification experiments that will stand the best chances to successfully express, purify and crystallize with little further intervention. Our method suggests that there are some 50 complexes recently discovered in yeast that could readily enter the structural biology pipelines.”
“This article concerns the kinetics, selectivity, and distribution of the Na(v)1.9, Na(v)1.8, and Na(v)1.7 channel subtypes in the CNS of the snail, Helix pomatia. Within the snail brain, Na(v)1.9- and Na(v)1.8-like channel subtypes are widely expressed, with particularly high levels in the pedal, cerebral, and buccal ganglia. The suboesophageal ganglion contains equal amounts of neurons labeled with Na(v)1.9, 1.8, and 1.7 antibodies.

Furthermore, VSV protein production in activated T cells is diminished by small interfering RNA-mediated eIF4E knockdown. These selleck compound results demonstrate that VSV replication in primary T lymphocytes relies on cell cycle transition from the G(0) phase to the G(1) phase, which is characterized by a sharp increase in ribogenesis and protein synthesis.”
“This study aimed to investigate the association of Parkinson’s

disease (PD) with dietary exposure to polychlorinated biphenyls (PCBs) and methylmercury (MeHg) in a community with increased exposure levels. A total of 79 clinically verified idiopathic PD cases and 154 controls matched by sex and age were examined in this case-control study in the Faroe Islands. Blood and hair samples were collected and a questionnaire recorded lifetime information

on residence, dietary habits, smoking history, and occupational exposure to solvents, pesticides, and metals. Both unconditional and conditional logistic regression analyses were used to estimate the odds ratio (OR) and 95% confidence interval (CI) in regard to relevant exposure variables. Increased ORs for dietary intakes of whale meat and blubber during adult life were statistically significant. The ORs for occupational exposure to solvents, pesticides and metals also suggested an increased risk for PD. Current serum concentrations of Sigma PCB and related contaminants suggested slightly increased ORs, although only beta-hexachlorocyclohexane (beta-HCH) was statistically significant. Increased intake of whale meat and blubber in adult life was significantly DZNeP nmr associated with PD, thus suggesting a positive association between previous exposure to marine food contaminants and development of PD. (C) 2008 Elsevier Inc. All rights reserved.”
“A rare Sindbis virus anti-E1 neutralizing monoclonal antibody, Sin-33, was investigated to determine

the mechanism of in vitro neutralization. A cryoelectron microscopic reconstruction of Sindbis virus (SVHR) neutralized with FAb from Sin-33 (FAb-33) revealed conformational changes on the surface of the virion at a resolution of 24 angstrom. FAb-33 was found to bind El in less than 1:1 molar ratios, as shown by the absence of FAb density in the reconstruction Glutamate dehydrogenase and stoichiometric measurements using radiolabeled FAb-33, which determined that about 60 molecules of FAb-33 bound to the 240 possible sites in a single virus particle. FAb-33-neutralized virus particles became sensitive to digestion by endoproteinase Glu-C, providing further evidence of antibody-induced structural changes within the virus particle. The treatment of FAb-33-neutralized or Sin-33-neutralized SVHR with low pH did not induce the conformational rearrangements required for virus membrane-cell membrane fusion. Exposure to low pH, however, increased the amount of Sin-33 or FAb-33 that bound to the virus particles, indicating the exposure of additional epitopes.

As participants with short-allele 5-HTTLPR genotypes may exhibit enhanced 5- HT vulnerability, this study examines the effects of tryptophan challenge on stress reactivity and performance in healthy participants with S’/S’ vs L’/L’ genotypes. Sixteen healthy subjects with homozygotic short alleles (S’/S’ = S/L(G), L(G)/L(G)) and 14 subjects with homozygotic long alleles (L’/L’ = L(A)/L(A)) of the 5-HTTLPR were tested

in a double-blind placebo-controlled design under acute stress exposure following tryptophan challenge or placebo. Although there were no 5-HTTLPR-related differences in stress responses, significant beneficial effects of tryptophan challenge on mood and stress performance were exclusively found in participants with S’/S’ genotypes. These findings suggest greater MK-1775 molecular weight brain 5- HT vulnerability to tryptophan manipulations

in participants with S’/S’ as compared with L’/L’ 5-HTTLPR genotypes. This apparent genetic 5- HT vulnerability may become a meaningful risk factor for depression when brain 5- HT falls below functional need in the face of real severe stressful life events. Neuropsychopharmacology (2009) 34, 2667-2674; doi:10.1038/npp.2009.92; published online 12 August 2009″
“The regional neuronal changes taking place in the early and late stages of antipsychotic treatment are still not well characterized in humans. In addition, it is not known whether these regional changes are predictive of or are correlated with treatment response. Using PET with (15)O, we evaluated the time course of regional cerebral blood flow (rCBF) patterns generated selleck kinase inhibitor by a first (haloperidol) and a second (olanzapine) generation antipsychotic drug in patients with schizophrenia during a 6-week treatment trial. Patients were initially scanned after withdrawal of all psychotropic medication (2 weeks), and then blindly randomized to treatment with haloperidol (n = 12) or olanzapine (n = 17) for a period of 6 weeks. Patients were scanned again after 1 and 6 weeks of

treatment. All assessments, including scanning sessions, were obtained in a double-blind manner. As hypothesized, we observed rCBF changes that were common to both the drugs, implicating cortico-subcortical and limbic neuronal networks in antipsychotic action. In addition, in these regions, some Mannose-binding protein-associated serine protease patterns seen at weeks 1 and 6 were distinctive, indexing neuronal changes related to an early (ventral striatum, hippocampus) and consolidated (anterior cingulate/medial frontal cortex) stage of drug response. Finally, both after 1 and 6 weeks of treatment, we observed differential patterns of rCBF activation between good and poor responders. After 1 week of treatment, greater rCBF increase in the ventral striatum and greater decrease in the hippocampus were associated with good response. Neuropsychopharmacology (2009) 34, 2675-2690; doi:10.1038/npp.2009.

However, scFvs typically show low thermal stability that limits their biomedical and biotechnological applications. In this study, we examined the thermal stability of the human and murine vascular endothelial growth factor antibody scFv fragment by molecular dynamics simulations. A consistent observation was the dissociation of the light-chain (VL) and heavy-chain (VH) domains and loss of the native

structures of both domains in the simulations at the elevated temperatures. The stability-limiting structural elements in the protein were revealed from the detailed analyses on the native contacts. We found that dissociation of the VL-VH domains was the first event leading to the unfolding of the native structure of the protein and the disruption of the VL-VH selleck kinase inhibitor interface was largely due to the break of the interfacial hydrophobic and aromatic interactions while the hydrogen-bonding interaction between Gln38 in VL and Gln39 in VH remained. Within the beta-barrel structure of the VL and VH domains, beta-strands beta 6, beta 2 and beta 11 appeared to be the least stable.

In addition, we found that the VH domain was more thermally resistant than the VL domain. Based on these findings, we discussed potential strategies to improve the stability of this therapeutically important scFv fragment.”
“Norovirus Aurora Kinase inhibitor genotype II.3 (GII.3) strains are a major cause of sporadic gastroenteritis. Intergenic recombination between the capsid and RNA-dependent Orotic acid RNA polymerase (RdRp) genes is common and results in the acquisition of an alternative

RdRp genotype. This study aimed to explore the evolution of the GII. 3 capsid gene, focusing on the influence of intergenic recombination. The capsid genes from six GII. 3 norovirus strains, collected from Australian children between 2001 and 2010, were sequenced and aligned with 66 GII. 3 capsid sequences from GenBank, spanning 1975 to 2010. The GII. 3 capsid gene evolved at a rate of 4.16 x 10(-3) to 6.97 x 10(-3) nucleotide substitutions/site/year from 1975 to 2010 and clustered into five temporally sequential lineages. Clustering of the GII. 3 capsid gene sequences was associated with intergenic recombination and switches between RdRp genotypes GII.3, GII.a, GII.b, GII.12, and an undefined ancestral RdRp. Comparison of the substitution rate of the GII. 3 and GII.b RdRps suggested that RdRp switching allows a higher evolutionary rate, leading to increased genetic diversity and adaptability. Alignment of GII. 3 capsid sequences revealed 36 lineage-specific conserved amino acid substitutions, four of which were under positive selection. Many conserved substitutions were within predicted antibody binding regions and close to host attachment factor binding sites. In conclusion, evolution of GII.

After further adjustment for baseline systolic blood pressure, history of diabetes, and total and HDL cholesterol, corresponding HRs were 1 07 (1.03-1.11) with BMI, 1.10 (1.05-1.14) with waist circumference, and 1.12 (1.08-1.15) with waist-to-hip ratio. Addition of information on BMI, waist circumference, or waist-to-hip ratio to a cardiovascular disease risk prediction model containing conventional risk factors did not importantly improve risk discrimination (C-index changes of -0.0001, -0.0001, and 0.0008, respectively), nor classification of participants to categories

of predicted 10-year risk (net reclassification improvement -0.19%, -0.05%, and -0.05%, respectively). Findings were similar when adiposity measures were considered buy Ro 61-8048 in combination. Reproducibility PSI-7977 mw was greater for BMI (regression dilution ratio 0.95, 95% CI 0.93-0.97) than for waist circumference (0.86, 0.83-0.89) or waist-to-hip ratio (0.63, 0.57-0.70).

Interpretation BMI, waist circumference, and waist-to-hip ratio, whether assessed singly or in combination, do not importantly improve cardiovascular disease risk prediction in people in developed countries when additional information is available

for systolic blood pressure, history of diabetes, and lipids.”
“Follow-up studies of eating disorders (EDs) suggest outcomes ranging from recovery to chronic illness or death, but predictors of outcome have not been consistently identified. We tested 5151 single-nucleotide polymorphisms (SNPs) in approximately 350 candidate genes for association with recovery from ED in 1878 women. Initial analyses focused on a strictly defined discovery cohort of women who were over age 25 years, carried a lifetime diagnosis of an ED, and for whom data were available regarding the presence (n = 361 ongoing symptoms in the past year, ie, ‘ill’) or absence (n = 115 no symptoms in the past year, ie, ‘recovered’) of ED symptoms. An intronic SNP (rs17536211) in GABRG1 showed the strongest statistical evidence of association (p = 4.63 x 10(-6), false discovery rate (FDR) = 0.021, odds ratio (OR) = 0.46). We replicated these findings in a more liberally defined cohort of women

age 25 years or younger (n = 464 ill, n = 107 recovered; p = 0.0336, OR = 0.68; combined sample p = 4.57 x 10(-6), FDR = 0.0049, OR = 0.55). Enrichment analyses revealed that GABA Rolziracetam (gamma-aminobutyric acid) SNPs were over-represented among SNPs associated at po0.05 in both the discovery (Z = 3.64, p = 0.0003) and combined cohorts (Z = 2.07, p = 0.0388). In follow-up phenomic association analyses with a third independent cohort (n = 154 ED cases, n = 677 controls), rs17536211 was associated with trait anxiety (p = 0.049), suggesting a possible mechanism through which this variant may influence ED outcome. These findings could provide new insights into the development of more effective interventions for the most treatment-resistant patients. Neuropsychopharmacology (2011) 36, 2222-2232; doi: 10.1038/npp.

During the recognition task, schizophrenia patients exhibited lower BOLD responses, less accuracy, and longer reaction times to famous and unfamiliar faces. Our results support the hypothesis that impaired face processing in schizophrenia

this website is related to early-stage deficits during the encoding and recognition of faces. (C) 2008 Elsevier Ireland Ltd. All rights reserved.”
“Adoptive immunotherapy with donor lymphocyte infusion (DLI) after allogeneic stem cell transplantation (alloSCT) may not only mediate Graft-versus-Leukemia (GvL) reactivity, but also induce Graft-versus-Host Disease (GvHD). As HLA-class II molecules are predominantly expressed on hematopoietic cells, CD4+ T cells may selectively mediate GvL reactivity without GvHD. Here, we assessed the capacity of human CD4+ T cells

to act as sole mediators of GvL reactivity in a NOD/scid mouse model for human acute lymphoblastic leukemia and chronic myeloid leukemia in lymphoid blast crisis. Highly purified CD4+ DLI eradicated the leukemic cells. The anti-tumor immunity was mediated by a polyclonal CD4+ T cell response comprising cytokine-producing T-helper and cytolytic T-effector cells directed against the mismatched HLA-class II molecules of the patients. Furthermore, primary leukemic cells acquired an antigen-presenting cell (APC) phenotype Amino acid in vivo after DLI, as well as in vitro Fedratinib research buy after co-culture with leukemia-specific CD4+ T cells. In conclusion, our results show that CD4+ T cells can be strong

mediators of anti-tumor immunity, and provide evidence that cross-talk between CD4+ T cells and leukemic cells is the basis for induction of leukemic cells with an APC phenotype. These data emphasize the clinical relevance of CD4+ T cell based immunotherapy as treatment modality for hematological malignancies after alloSCT. Leukemia (2012) 26, 312-322; doi:10.1038/leu.2011.222; published online 23 August 2011″
“The lateral ventricle in adult mammalian brain is widely acknowledged as one of the areas that undifferentiated neural cells such as neural stem cells and neural progenitor cells inhabit. However, immunological aspects of neural stem cells in the lateral ventricle are still under debate. Here, we report the generation and characterization of a novel monoclonal antibody (mAb), called Namu mAb, which stains the subventricular zone in the lateral ventricle of adult mouse brain. Namu mAb reacted to the cells in the subventricular zone and never reacted to differentiated neural cells such as neurons and glial cells such as astrocytes and oligodendrocytes. Its reaction pattern for the subventricular zone and the neurospheres was similar to that of Nestin and glial fibrillary acidic protein mAbs.

Here we report the results of employing an alternative strategy that specifically Selleckchem SB273005 addresses the conformational stability of PrPSc and that has been used previously to characterize animal prion strains transmitted to rodents. The results show that there are at least two distinct conformation stability states in human prion diseases, neither of which appears to correlate fully with the PrPres type, as judged by fragment size or glycosylation, the PRNP codon 129 status, or the presence or absence of mutations in PRNP. These results suggest that conformational stability represents a further

dimension to a complete description of potentially phenotype-related properties of PrPSc in human prion diseases.”
“Gammaherpesviruses are important oncogenic pathogens that transit between lytic and

latent life cycles. Silencing the lytic gene expression program enables the establishment of latency and a lifelong chronic infection of the host. In murine gammaherpesvirus 68 (MHV68, gamma HV68), essential lytic switch gene 50 controls the interchange between lytic and latent gene expression programs. However, negative regulators of gene 50 expression remain largely undefined. We report that the MHV68 lytic cycle is silenced in infected LOXO-101 in vivo macrophages but not fibroblasts and that histone deacetylases (HDACs) mediate silencing. The HDAC inhibitor trichostatin A (TSA) acts on the gene 50 promoter to induce lytic replication of MHV68. HDAC3, HDAC4, and the nuclear receptor corepressor (NCoR) are required for efficient silencing of gene 50 expression. NCoR is critical for transcriptional repression of cellular genes by unliganded nuclear receptors. Retinoic acid, a known ligand for the NCoR complex, derepresses gene 50 expression and enhances MHV68 lytic replication. Moreover, HDAC3, HDAC4, and NCoR act on the gene 50 promoter and are recruited to this promoter in a retinoic acid-responsive manner. We provide the first example of NCoR-mediated, HDAC-dependent regulation of viral gene expression.”
“Hepatitis

C virus (HCV) is a causative agent of chronic Decitabine solubility dmso hepatitis, liver cirrhosis, and hepatocellular carcinoma. HCV in circulating blood associates with lipoproteins such as very low density lipoprotein (VLDL) and low-density lipoprotein (LDL). Although these associations suggest that lipoproteins are important for HCV infectivity, the roles of lipoproteins in HCV production and infectivity are not fully understood. To clarify the roles of lipoprotein in the HCV life cycle, we analyzed the effect of apolipoprotein E (ApoE), a component of lipoprotein, on virus production and infectivity. The production of infectious HCV was significantly reduced by the knockdown of ApoE.

Ten trained, non-heat acclimated males performed two 1 h run on treadmill at 60% VO2max in neutral (22 +/- 1 degrees

C, 50 Selleckchem YM155 +/- 5RH) and hot (35 +/- 1 degrees C, 50 +/- 5) temperature conditions. Samples of the venous blood were taken (Pre, post, 2 h post) for determination of serum IL-17, cortisol concentrations and numbers of leukocytes and neutrophils. In addition, body temperature, RPE and PVC during exercise were measured. The collected data were analyzed using the Repeated-Measures analyses of variance and Bonferroni post hoc and Paird T tests (p < 0.05). The concentration of cortisol and total number of leukocytes increased significantly after exercise, in both conditions (p < 0.0001) and were significantly higher in hot than neutral (p = 0.016, p = 0.002). During the rest period (2 h post) the number of neutrophils increased significantly in hot environment (p = 0.018). The concentrations of

IL-17 increased significantly only after exercise in hot (p < 0.0001) and were significantly higher during hot than neutral (p = 0.002). The results suggest that exercise in hot environment cause increase in body temperature, perceived exertion and cardiac-vascular changes which are sufficient to elicit immune, hormonal and inflammatory responses. The present results confirm the additive effect of heat stress on the IL-17 response during exercise. (C) 2011 Elsevier Ltd. All rights reserved.”
“BACKGROUND

The majority of Death with Dignity participants

in Washington selleck chemicals State and Oregon have received a diagnosis of terminal cancer. As more states consider legislation regarding physician-assisted death, the experience of a comprehensive cancer center may be informative.

METHODS

We describe the implementation of a Death with Dignity program at Seattle Cancer Care Alliance, the site of care for the Fred Hutchinson-University of Washington Cancer Consortium, a comprehensive cancer center in Seattle that serves the Pacific Northwest. Institution-level data were compared with publicly available state-wide data from Oregon and Washington.

RESULTS

A total of 114 patients inquired about our Death with Dignity program between Edoxaban March 5, 2009, and December 31, 2011. Of these, 44 (38.6%) did not pursue the program, and 30 (26.3%) initiated the process but either elected not to continue or died before completion. Of the 40 participants who, after counseling and upon request, received a prescription for a lethal dose of secobarbital (35.1% of the 114 patients who inquired about the program), all died, 24 after medication ingestion (60% of those obtaining prescriptions). The participants at our center accounted for 15.7% of all participants in the Death with Dignity program in Washington (255 persons) and were typically white, male, and well educated. The most common reasons for participation were loss of autonomy (97.2%), inability to engage in enjoyable activities (88.

The data presented here thus suggest a novel mechanism by which herpesviral protein kinases suppress host innate immune responses and facilitate virus replication.”
“Repeated, intermittent exposure to the psychomotor stimulants amphetamine

and cocaine induces a progressive and enduring augmentation of their locomotor-activating effects, known as behavioral sensitization, which is accompanied by similarly stable adaptations in the dendritic structure of cortico-striatal neurons. We examined whether repeated exposure to the increasingly abused amphetamine derivative 3,4-methylenedioxymethamphetamine (MDMA; ecstasy) also results in long-lasting behavioral and morphological changes in mesocortical (medial prefrontal cortex) and ventral striatal (nucleus accumbens) neurons. Rats received two daily injections of either 5.0 mg/kg (+/-)-MDMA or saline BIX 1294 price vehicle, similar to 6 h apart, for 3 consecutive days, followed Angiogenesis inhibitor by 4 drug-free days for a total of 3 weeks. Following a 4-week drug-free period, MDMA-pretreated rats displayed behavioral sensitization, as well as large increases in spine density and the number of multiple-headed spines on medium spiny neurons in core and shelf subregions of nucleus accumbens. In medial prefrontal cortex, the

prelimbic subregion showed increased spine density on distal dendrites of layer V pyramidal neurons, while the anterior cingulate subregion showed a change in the distribution of dendritic material instead. Collectively, our results show that long-lasting locomotor sensitization to MDMA is accompanied by reorganization of synaptic connectivity in limbic-cortico-striatal circuitry. The differential plasticity in cortical subregions, moreover, suggests that drug-induced structural changes are not homogeneous and may be specific to the circuitry underlying long-term changes in

drug-seeking and drug-taking behavior. (C) 2009 IBRO. Published by Elsevier Ltd. All rights reserved.”
“We have previously described a novel flavivirus vaccine technology based on a single-cycle, capsid (C) gene-deleted flavivirus called RepliVAX. RepliVAX can be propagated in cells that express high levels of C but undergoes Oxaprozin only a single cycle of infection in vaccinated hosts. Here we report that we have adapted our RepliVAX technology to produce a dengue vaccine by replacing the prM/E genes of RepliVAX WN (a West Nile virus [WNV] RepliVAX) with the same genes of dengue virus type 2 (DENV2). Our first RepliVAX construct for dengue virus (RepliVAX D2) replicated poorly in WNV C-expressing cells. However, addition of mutations in prM and E that were selected during blind passage of a RepliVAX D2 derivative was used to produce a second-generation RepliVAX D2 (designated D2.2) that displayed acceptable growth in WNV C-expressing cells. RepliVAX D2.

538 ms) and for conflict ratio (0.158 vs. 0.191). The latter difference mainly resulted from gender-specific variances of the conflict network

in opposite directions. The executive function as represented by the conflict network of visual attention of the ANT is affected in schizophrenia. We have detected hitherto unreported gender-specific differences between healthy controls and schizophrenic patients. Especially as regards the conflict network, the ANT offers a promising methodology to detect a neuropsychological endophenotype of schizophrenia. (C) 2008 Elsevier Ireland Ltd. All rights reserved.”
“Humoral immune responses are thought to play a major role in dengue virus-induced immunopathology; however, little is known about the plasmablasts producing NCT-501 supplier these antibodies during an ongoing infection. FRAX597 Herein we present an analysis of plasmablast responses in patients with acute dengue virus infection. We found very potent plasmablast responses that often increased more than 1,000-fold over the baseline levels in healthy volunteers.

In many patients, these responses made up as much 30% of the peripheral lymphocyte population. These responses were largely dengue virus specific and almost entirely made up of IgG-secreting cells, and plasmablasts reached very high numbers at a time after fever onset that generally coincided with the window where the most serious dengue virus-induced pathology is observed. The presence

of these large, rapid, and virus-specific plasmablast responses raises the question as to whether these cells might have a role in dengue immunopathology during the ongoing infection. These findings clearly illustrate the need for a detailed understanding of the repertoire and specificity of the antibodies that these plasmablasts produce.”
“Recent literature suggests that lying may be revealed by elevated cognitive effort. A functional magnetic resonance imaging experiment using a match-mismatch detection task was conducted that found tuclazepam support for this hypothesis in two ways. First, compared to truthful reporting, lying (i.e., responding that matches were mismatches or vice versa) triggered greater activation of the working memory network in the brain. This was especially true for lying about a match, where activation in the WM network was found to be greater than when lying about a mismatch. Lying also activated the right rostrolateral prefrontal cortex (BA 10) a key cognitive control region that regulates the interplay between stimulus-oriented and internally-generated schemas. Second, activation in the right inferior frontal gyrus (BA 44) – a brain region underpinning inhibition – predicted lying skill. The findings show that the neural correlates of cognitive effort and control can be used to detect lying, and that a specific neural marker of inhibition can predict how well one lies.