From sensory processes to conscious perception

In recent years, cognitive neuroscientists have began to explore the process of how sensory information gains access to awareness. To further probe this process, event-related functional magnetic resonance imaging (fMRI) was used while testing subjects with a paradigm known as the "attentional blink." In this paradigm, visually presented information sporadically fails to reach awareness. It was found that the magnitude and time course of activation within the anterior cingulate (BA 32), medial prefrontal cortex (BA 9), and frontopolar cortex (BA 10) predicted whether or not information was consciously perceived during the critical period for the attentional blink. These results are discussed in light of a neural framework for conscious processing.     

Social science as dialogue: narcissism,individualist and collectivist values,and religious interest in iran and the united states

This investigation most importantly sought to illustrate the use of social science to promote cross-cultural dialogue. Fukuyama (1992) explained contemporary cultural trends in terms of a triumphant individualism that would overcome all other forms of social life, including what he described as the “fundamentalist resentment” of Iran. Lasch (1979) more pessimistically diagnosed Western social arrangements in terms of an emerging “culture of narcissism.” In this study, Iranian and American university students responded to measures of narcissism, individualist and collectivist values, religious interest, and psychological adjustment (identity, self-actualization, and self-consciousness). Variables related to a sense of community (collectivist values, religious interest, and identity) correlated negatively with narcissism in both societies, as did self-actualization. These data supported a moderate position between the polarized extremes of Fukuyama and Lasch and more importantly demonstrated how social scientific methods might be useful in creating a “space” for conducting a “dialogue between civilizations.”     

Analyzing the Process and Content of Genetic Counseling in Familial Breast Cancer Consultations

A detailed examination of the process of genetic counseling has been identified as a priority area for research by previous authors. This multicenter longitudinal study examined the process and content of genetic counseling in initial consultations with women from high-risk breast cancer families. One hundred and fifty-eight consultations with women unaffected and affected with breast cancer were audio taped and transcribed verbatim. A detailed coding system was developed. Clinical geneticists and genetic counselors demonstrated consistently good practice in giving detailed information on essential aspects related to familial breast cancer such as screening and management, genetic testing, breast cancer genetics, and prophylactic surgery. Eliciting emotional concerns and facilitating communication were found to be inconsistently present. As clinical practice guidelines and the general communication literature emphasize the importance of these factors, this is an area where training in or self-monitoring of such behaviors may assist consultants to further develop these skills.     

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.     

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.     

The clinical efficacy and safety of galantamine in the treatment of Alzheimer's disease

Alzheimer's disease is a progressive, neurodegenerative condition characterized by deficits in cognition, inability to perform activities of daily living, and alterations in behavior. Galantamine hydrobromide is the newest acetylcholinesterase inhibitor (AChEI) approved in the United States for the treatment of mild-to-moderate AD. The safety and efficacy of galantamine has been demonstrated in multiple randomized, Phase III trials of >2,600 patients with mild-to-moderate AD. Studies have found that galantamine improved or maintained performance in all domains of AD (cognition, function, behavior, and caregiver burden) in the short term and slowed the decline in performance or maintained baseline performance through 12 months. The dual mechanism of action may make galantamine a reasonable treatment option for both newly diagnosed patients and patients who have not benefitted from or have poorly tolerated current therapy.