Female physical attractiveness in Britain and Malaysia: a cross-cultural study

Two purported cues to perceived female physical attractiveness are body mass index (BMI) and body shape as measured by the waist-to-hip ratio (WHR). This study examined the relative contribution of both cues in several culturally socio-economically distinct populations. Six hundred and eighty-two participants from Britain and Malaysia were asked to rate a set of images of real women with known BMI and WHR. The results showed that BMI is the primary determinant of female physical attractiveness, whereas WHR failed to emerge as a significant predictor. The results also showed that there were significant differences in preferences for physical attractiveness along a gradient of socio-economic development, with urban participants preferring images of women with significantly lower BMIs than their rural counterparts. The findings are discussed in terms of evolutionary psychological explanations of mate selection, and sociocultural theory, which emphasises the learning of preferences for body sizes in social and cultural contexts.     

Coming to terms with risk factors for eating disorders: application of risk terminology and suggestions for a general taxonomy

The aims of the present review are to apply a recent risk factor approach (H. C. Kraemer et al., 1997) to putative risk factors for eating disorders, to order these along a timeline, and to deduce general taxonomic questions. Putative risk factors were classified according to risk factor type, outcome (anorexia nervosa, bulimia nervosa, binge-eating disorder, full vs. partial syndromes), and additional factor characteristics (specificity, potency, need for replication). Few of the putative risk factors were reported to precede the onset of the disorder. Many factors were general risk factors; only few differentiated between the 3 eating disorder syndromes. Common risk factors from longitudinal and cross-sectional studies were gender, ethnicity, early childhood eating and gastrointestinal problems, elevated weight and shape concerns, negative self-evaluation, sexual abuse and other adverse experiences, and general psychiatric morbidity. Suggestions are made for the conceptualization of future risk factor studies.     

Effects of binding in the identification of objects

The binding problem requires a solution at the level of individual neurons, but no definite mechanism has yet be given. Therefore, the neuronal level is as yet inadequate for modeling cognitive processes in which binding plays a crucial role. Moreover, the neuronal level involves too many details that are unlikely to be essential for understanding cognition. A general model of cognitive brain functioning is described in which cognitive tasks are represented in a network of cell assemblies. In the network, binding is functionally defined in a way that is compatible with the neuronal level. A computer simulation of the model clarifies how the binding of location and identity of a set of simultaneously presented letters takes place and how questions about the location and identity of the letters are answered. From the simulation of the task three predictions on the logistics of neural processes are derived: 1. When the cell assembly representing a letter participates in more than one temporary excitation loop, it will reach its critical threshold faster. At the behavioral level this means that as the number of identical letters in the display increases, responses will be faster. 2. In order to answer questions about the location and identity of presented letters cell assemblies representing the target location and the target identity have to become bound to their appropriate values. As a consequence the facilitatory effect of identical letters will be stronger if they involve the target location or the target identity than when identical non-targets are involved. 3. Negative identifications are more dependent on the presentation time of the letters than positive identifications because the excitation loops involved take more time to reach the critical threshold. Therefore, the facilitatory effect of identical letters is stronger when the external activation is relatively strong, i.e., when presentation time of the letters is sufficiently long. The reaction times obtained in three behavioral experiments support these hypotheses. Effects of binding can therefore be predicted on the basis of the general logistics of neural processes, without assumptions about a specific binding mechanism at the neuronal level.     

Actions blind to conceptually overlapping stimuli

Participants are worse at identifying spatial symbols (arrowheads) while performing spatially compatible manual key presses. The present experiments investigated the generality of this blindness effect to response-compatible stimuli. In Experiment 1 a left key press deteriorated the identification of left-pointing arrows, and a right key press deteriorated the perception of right-pointing arrows, independent of the hands used to press the key. Thus the blindness effect is based on codes of the distal response location rather than on the body-intrinsic anatomical connection of the hands. Experiment 2 extended the blindness effect to verbal responses and written position words (left, right, up, down). Vocalizing a position word blinded to directly compatible position words (e.g., left-left), but not to orthogonally compatible position words (e.g., left-down). This result suggests that the use of identical stimulus-response codes, and not the use of saliency-matching but distinct codes, suffices to produce blindness effects. Finally, Experiment 3 extended the blindness phenomenon beyond the spatial domain by demonstrating blindness between saying color words and perceiving color patches. Altogether, the experiments revealed action-induced blindness to be a phenomenon of broad empirical validity occurring whenever action and perception afford simultaneous access to the same conceptual codes.     

Perceiving while acting: action affects perception

In two experiments we studied how motor responses affect stimulus encoding when stimuli and responses are functionally unrelated and merely overlap in time. Such R-S effects across S-R assignments have been reported by Schubö, Aschersleben, and Prinz (2001), who found that stimulus encoding was affected by concurrent response execution in the sense of a contrast (i.e., emphasizing differences). The present study aimed at elucidating the mechanisms underlying this effect. Experiment 1 studied the time course of the R-S effect. Contrast was only obtained for short intertrial intervals (ITIs). With long ITIs contrast turned into assimilation (i.e., emphasizing similarities). Experiment 2 excluded an interpretation of the assimilation effect in terms of motor repetition. Our findings support the notion of a shared representational domain for perception and action control, and suggest that contrast between stimulus and response codes emerges when two S-R assignments compete with each other in perception. When perceptual competition is over, assimilation emerges in memory.     

Spatial learning in rats is impaired by microinfusions of protein kinase C-gamma antisense oligodeoxynucleotide within the nucleus accumbens

The nucleus accumbens (NAcc) has been shown to play a role in motor and spatial learning. Protein kinase C (PKC) has been implicated in the mechanisms of initiation and maintenance of long-term potentiation that is thought to be involved in the storage of long-term memory. In the present study, the importance of de novo synthesis of PKC-gamma within the NAcc in the acquisition and retention of spatial discrimination learning was assessed using an antisense knockdown approach. Separate groups of Long-Evans rats were exposed to acute microinfusions (6microg/microl) of PKC-gamma antisense oligodeoxynucleotide (AS-ODN), control oligodeoxynucleotide (C-ODN) or vehicle into the NAcc at 24 and 3h before each training session. Behavioral findings showed that the blockade of NAcc-PKC-gamma translation caused impairments in the early phase of learning and retention of spatial information. Biochemical experiments showed that PKC-gamma expression was reduced and Ca(2+)/phospholipid-dependent protein kinase C (PKC) activity was blocked significantly in the AS-ODN-treated rats in comparison with control rats. The present findings suggest that NAcc-PKC-gamma plays a role during the early acquisition of spatial learning. Also, retention test results suggest that NAcc-PKC-gamma may be working as an intermediate factor involved in the onset of molecular mechanisms necessary for spatial memory consolidation within the NAcc.     

Extinction-induced immobility in the water maze and its neurochemical concomitants in aged and adult rats: a possible model for depression?

Extinction of escape behavior in the water maze due to the removal of the platform, was hypothesized to induce a negative state, including the development of immobility, which is held to reflect a state of "despair" when measured in the forced swimming test. 27 aged and 8 adult animals (26 and 3 months old Wistar rats, respectively) were tested in the water maze during nine days with a platform hidden, followed by 7 days of extinction trials with the platform absent. As expected, both age groups developed immobility over the extinction trials, with the aged showing more than the adults. To examine whether the age difference in immobility was related to performance differences during acquisition, the aged were subdivided into superior, intermediate and inferior learners (n = 9 per group) on the basis of overall times to platform during acquisition, and compared with each other and the adults. Results showed that the aged inferior learners displayed the highest levels of immobility among the aged. Immobility scores were then correlated with post-mortem neurotransmitter contents in the hippocampus and ventral striatum. In the ventral striatum, levels of immobility were correlated with levels of acetylcholine, dopamine and the metabolite dihydroxyphenylacetic acid in the aged, and with norepinephrine in the adults. The data support the hypothesis that multiple extinction trials in the water maze result in immobility that may indicate "behavioral despair," and that striatal neurotransmitter systems correlate with the degree of its expression. The concept of extinction-induced despair is held to provide the promise of a conceptual and empirical model of human depression that is the consequence of loss of reinforcers.     

Is the unilateral lesion of the left substantia nigra pars compacta sufficient to induce working memory impairment in rats?

Adult male Wistar rats with a substantia nigra pars compacta (SNc) lesion induced by intranigral administration of 1 micromol 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) were used as a model of early phase Parkinson's disease (PD). This lesion caused a partial depletion of striatal dopamine (DA). The animals were submitted to a spatial working memory version of the water maze task in which they had to find a hidden (submersed) platform using online-maintained information that the platform remains in the same place during four consecutive trials, but that it is moved to another place every training day. Left, but not right SNc-lesioned rats were impaired in finding the platform in the second trial. This result suggests that the left SNc plays a key role in spatial working memory. Control experiments ruled out the possibility that motor impairment, sensory neglect, and/or impairment in the mental representation of the contralateral spatial environment had affected performance of the SNc-lesioned rats.     

Identifying environmental contributions to autism: provocative clues and false leads

The potential role of environmental factors in autism spectrum disorders (ASD) is an area of emerging interest within the public and scientific communities. The high degree of heritability of ASD suggests that environmental influences are likely to operate through their interaction with genetic susceptibility during vulnerable periods of development. Evaluation of the plausibility of specific neurotoxicants as etiological agents in ASD should be guided by toxicological principles, including dose-effect dependency and pharmacokinetic parameters. Clinical and epidemiological investigations require the use of sufficiently powered study designs with appropriate control groups and unbiased case ascertainment and exposure assessment. Although much of the existing data that have been used to implicate environmental agents in ASD are limited by methodological shortcomings, a number of efforts are underway that will allow more rigorous evaluation of the role of environmental exposures in the etiology and/or phenotypic expression of the disorder. Surveillance systems are now in place that will provide reliable prevalence estimates going forward in time. Anticipated discoveries in genetics, brain pathology, and the molecular/cellular basis of functional impairment in ASD are likely to provide new opportunities to explore environmental aspects of this disorder.