Memory‐Based Deception Detection: Extending the Cognitive Signature of Lying From Instructed to Self‐Initiated Cheating

From a cognitive perspective, lying can be regarded as a complex cognitive process requiring the interplay of several executive functions. Meta‐analytic research on 114 studies encompassing 3,307 participants (Suchotzki, Verschuere, Van Bockstaele, Ben‐Shakhar, & Crombez, 2017) suggests that computerized paradigms can reliably assess the cognitive burden of lying, with large reaction time differences between lying and truth telling. These studies, however, lack a key ingredient of real‐life deception, namely self‐initiated behavior. Research participants have typically been instructed to commit a mock crime and conceal critical information, whereas in real life, people freely choose whether or not to engage in antisocial behavior. In this study, participants (n = 433) engaged in a trivia quiz and were provided with a monetary incentive for high accuracy performance. Participants were randomly allocated to either a condition where they were instructed to cheat on the quiz (mimicking the typical laboratory set‐up) or to a condition in which they were provided with the opportunity to cheat, yet without explicit instructions to do so. Assessments of their response times in a subsequent Concealed Information Test (CIT) revealed that both instructed cheaters (n = 107) and self‐initiated cheaters (n = 142) showed the expected RT‐slowing for concealed information. The data indicate that the cognitive signature of lying is not restricted to explicitly instructed cheating, but it can also be observed for self‐initiated cheating. These findings are highly encouraging from an ecological validity perspective.     

Reduced Levels of Vasopressin and Reduced Behavioral Modulation of Oxytocin in Psychotic Disorders

Oxytocin (OT) and arginine vasopressin (AVP) exert robust influence on social affiliation and specific cognitive processes in healthy individuals. Abnormalities in these neuroendocrine systems have been observed in psychotic disorders, but their relation to impairments in behavioral domains that these endocrines modulate is not well understood. We compared abnormalities of OT and AVP serum concentrations in probands with schizophrenia (n = 57), schizoaffective disorder (n = 34), and psychotic bipolar disorder (n = 75); their first-degree relatives without a history of psychosis (n = 61, 43, 91, respectively); and healthy controls (n = 66) and examined their association with emotion processing and cognition. AVP levels were lower in schizophrenia (P = .002) and bipolar probands (P = .03) and in relatives of schizophrenia probands (P = .002) compared with controls. OT levels did not differ between groups. Familiality estimates were robust for OT (h ² = 0.79, P = 3.97e−15) and AVP (h ² = 0.78, P = 3.93e−11). Higher levels of OT were associated with better emotion recognition (β = 0.40, P < .001) and general neuropsychological function (β = 0.26, P = .04) in healthy controls as expected but not in any proband or relative group. In schizophrenia, higher OT levels were related to greater positive symptom severity. The dissociation of OT levels and behavioral function in all proband and relative groups suggests that risk and illness factors associated with psychotic disorders are not related to reduced OT levels but to a disruption in the ability of physiological levels of OT to modulate social cognition and neuropsychological function. Decreased AVP levels may be a marker of biological vulnerability in schizophrenia because alterations were seen in probands and relatives, and familiality was high.Key words: oxytocin, vasopressin, schizophrenia, bipolar disorder, emotion recognition     

Hirschsprung's disease associated enterocolitis: A comprehensive review

Hirschsprung’s disease (HSCR) is a congenital disorder characterized by failure of the neural crest cells to migrate and populate the distal bowel during gestation affecting different lengths of intestine leading to a distal functional obstruction. Surgical treatment is needed to correct HSCR once the diagnosis is confirmed by demonstrating the absence of ganglion cells or aganglionosis of the affected bowel segment. Hirschsprung’s disease associated enterocolitis (HAEC) is an inflammatory complication associated with HSCR that can present either in the pre- or postoperative period and associated with increased morbidity and mortality. The pathogenesis of HAEC remains poorly understood, but intestinal dysmotility, dysbiosis and impaired mucosal defense and intestinal barrier function appear to play a significant role. There is no clear definition for HAEC, but the diagnosis is primarily clinical, and treatment is guided based on severity. Here, we aim to provide a comprehensive review of the clinical presentation, etiology, pathophysiology, and current therapeutic options for HAEC.     

POTENTIATION OF THE T-LYMPHOCYTE RESPONSE TO MITOGENS : I. THE RESPONDING CELL

Human and mouse lymphoid cells, stimulated by phytohemagglutinin (PHA) or lipopolysaccharide W (LPS), release supernatant factor(s) which are mitogenic for mouse thymocytes and which potentiate their responses to PHA or concanavalin A (Con A), The term LAF (lymphocyte-activating factor) is proposed for this activity. LAF not only enhances the mitotic responses of the less dense thymus subpopulations (A, B, and C) separable on discontinuous bovine serum albumin (BSA) gradients but also gives substantial responses in the otherwise inert cells of the denser fractions D and P. LAF does not exert a potentiating stimulatory effect on the responses of unfractionated mouse spleen cells, but does act synergistically with PHA on nonadherent spleen cells and on spleen cells of mice of several strains 5 days after irradiation and injection of thymocytes. Similarly LAF, which has no visible effect on unfractionated human peripheral blood cells, strongly potentiates the PHA response of column-purified lymphocytes, when these are cultured at low concentration. We conclude that LAF stimulates both central and peripheral T lymphocytes and enhances their responses to other stimulants.     

Effect of cortisone treatment on the active transport of calcium by the small intestine

It is generally recognized that glucocorticoid administration may diminish calcium absorption in vivo as well as the active transport of calcium by the intestine in vitro. Recent studies by others have emphasized the possibility of an alteration in the metabolism of vitamin D to 25-hydroxycholecalciferol in accounting for the steroid effects on calcium absorption. The results obtained in the present studies fail to support this hypothesis.The present studies confirm that the administration of cortisone or other glucocorticoids to the rat interferes with the active transport of calcium by duodenal gut sacs in vitro. This abnormality is not due to an alteration in the permeability of the intestine to calcium, and it cannot be corrected by the administration of either massive doses of vitamin D(2) or modest doses of 25-hydroxycholecalciferol. Experiments concerned with the effects of cortisone on the level of the vitamin D-dependent duodenal calcium-binding protein, the amount of bioassayable vitamin D activity in the mucosa, and the distribution and metabolism of (3)H-vitamin D(3), did not provide evidence in favor of a harmone-related defect in either the localization of vitamin D or its metabolism to 25-hydroxycholecalciferol. Alterations in the transport of iron and D-galactose, not dependent on vitamin D, suggest that cortisone treatment may be responsible for more than a simple antagonism to the effects of vitamin D.The results of the present studies indicate that cortisone administration affects the cellular mechanisms mediating calcium transport in a manner that is opposite to the effects of vitamin D, but seems to be independent of any direct interaction with the parent vitamin or its metabolites. If a disorder in vitamin D metabolism is at all involved, it is at a step subsequent to 25-hydroxylation.     

Frequency of health service use in the year prior to asthma death

Objective: High frequency health service use (HSU) is associated with poorly controlled asthma, and is a recognized risk factor for near-fatal or fatal asthma. The objective of this study was to describe the frequency of HSU in the year prior to asthma death. Methods: Individuals aged 0–99 years who died from asthma from April 1996 to December 2011 in Ontario, Canada were identified as cases. Cases were matched to 4–5 live asthma controls by age, sex, rural/urban residence, socioeconomic status, duration of asthma and a co-diagnosis of COPD. HSU records in the year prior to death [hospitalization, emergency department (ED) and outpatient visits] were assembled. The association of prior HSU and asthma death was measured by conditional logistic regression models. Results: From 1996 to 2011, 1503 individuals died from asthma. While the majority of cases did not have increased HSU as defined in the study, compared to matched live asthma controls, the cases were 8-fold more likely to have been hospitalized two or more times (OR?=?7.60; 95% CI: 4.90, 11.77), 13-fold more likely to have had three or more ED visits (OR?=?13.28; 95% CI: 7.55, 23.34) and 4-fold more likely to have had five or more physician visits for asthma (OR?=?4.41; 95% CI: 3.58, 5.42). Conclusions: Frequency of HSU in the year prior was substantially higher in those died from asthma. Specifically, more than one asthma hospital admission, three ED visits or five physician visits increased the asthma mortality risk substantially and exponentially.     

Ethical issues in the use of genetic information

Ethical issues in the use of genetic information

All authors

Stephen H. Dinwiddie, Jinger Hoop & Elliot S. Gershon

https://doi.org/10.1080/09540260400014427

Published online:

11 July 2009

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