The results suggest a role of BDNF in prefrontal cognitive function in bipolar illness. The tests of prefrontal cognition may be considered as endophenotypic markers in bipolar illness.

A higher degree of cognitive dysfunction connected with frontal lobe activity during an acute depressive episode was found in bipolar compared with unipolar depressed patients. These results may corroborate other findings pointing to pathogenic distinctions between bipolar and unipolar affective illness and to some similarities between bipolar illness and schizophrenia.

The measures of prefrontal cognition have been used as endophenotype in molecular-genetic studies. Brain-derived neurotrophic factor (BDNF) has been implicated in cognitive functions and in the pathogenesis of major psychoses. No relationship between BDNF polymorphism and the results of the N-back test was found in this group. A limitation to the results could be variable psychopathological state and medication during cognitive testing and lack of Hardy-Weinberg equilibrium in schizophrenia group. Val66Met polymorphism of the BDNF gene may be associated with cognitive performance on the WCST in bipolar mood disorder but not in schizophrenia. An association of this polymorphism with performance on the Nback test in schizophrenia and not in bipolar illness may suggest that in schizophrenia, the BDNF system may be connected with early phases of information processing.

small number of heterozygotes were present in the genotyped sample (n = 18) we excluded these individuals from further analysis.Examination of relative MD frequencies in each homozygous genotype group showed that the less prevalent T allele (the termination allele) was associated with an increased prevalence of MD (65% relative to 48%) in both sexes. Likewise, Neuroticism score (arcsine-transformed and age-regressed) was also found to be elevated in TT homozygotes, although this difference did not reach statistical significance (f = 3.0 1 , P = 0.08). Marker rs12520799 is located in dendritic cell nuclear protein 1 (DCNP1) on chromosome 5 where it yields a premature termination of translation at codon number 117. DCNP1 is expressed in both human brain and skeletal muscle, where it localises to the perinucleus of mature, and to a lesser extent immature dendritic cells.9 These cells moderate antigen-specific T-cell immunity 10 in a maturationdependent manner. 11,12 No information is available at present regarding structure-specific expression patterns of DCNP1 within the brain. DCNP1 is a novel candidate gene for MD that requires independent replication in a large sample. However, the observed effect of this premature termination variant is small compared with the large displacements typically associated with premature termination mutations in mendelian disease traits. Consequently, it remains unclear whether the approach described here is likely to represent a productive strategy for complex trait dissection.

Implantable gentamicin-collagen sponges significantly reduce the risk of sternal wound infection after cardiac surgery, with evidence consistent in randomized and observational-level data. However, the extent of this benefit might be attenuated in patients receiving bilateral internal thoracic artery grafts.